Pathway 3: Gastrointestinal/Abdominal Emergencies
(Adult and Pediatric)
The team continues the resuscitation along the pathway suggested by the initial clinical impression. Each pathway includes a complete, thorough, and rapid physical examination with additional history taking. The team leader is wary of conditions that may not be apparent. To obtain additional clinical data or to correct a missed or newly developed condition, the team leader repeats the initial survey if the patient is not responding satisfactorily.
Gastrointestinal (GI) emergencies can cause abdominal pain, bleeding, or sepsis. Order a chest x-ray as well as a flat plate abdominal x-ray. (If the patient is stable enough, take the chest x-rays in the upright position and also obtain an upright abdominal x-ray.)
Vomiting Blood
The source of
the hemorrhage may be esophageal, duodenal, or gastric. Examine for the
stigmata of liver cirrhosis: spider nevi, icterus, ascites, or enlarged
liver that may suggest esophageal varices. Ask about a history of
alcoholism or hepatitis as a cause of liver disease. Seek a history of
food intolerance, use of aspirin, and NSAID or epigastric pain typical
of gastritis or peptic ulcer disease.
Bleeding Esophageal Varices
Assume
that variceal bleeding is likely to be occurring if there is evidence
of severe liver disease. If the patient is bleeding massively, approach
the problem aggressively. (Vol III—GI/AB1 Esophageal Varicies)
Initial Management
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Airway protection is needed. Prepare to keep the airway clear with suction. RSI with orotracheal intubation may be needed as soon as you establish IVs. (Vol II—Air Skills 4 Rapid Sequence Intubation)
Establish 2 large gauge IV lines. Begin volume replacement starting with a 1 to 2 liter bolus of saline IV in an adult and (PEDS) 10 to 20 mL/kg in children. Begin blood replacement early to avoid hemodilution and further hypocoagulopathy.
Establish central venous access (Vol II—Circ Skills 2 Central Venous Access) for monitoring central venous pressure. (Vol II—Circ Skills 3 Central Venous Pressure Measurement)
Assess coagulation status: If the patient demonstrates a hypocoagulable state (bleeding from needle puncture sites, etc), assess (PT, PTT, platelet count, bleeding time, and clinical evidence of abnormal clotting) and treat coagulopathies induced by medications, disease states, or bleeding/ transfusions. Treatment may include Vitamin K 10 to 15 U IM or SQ. Vitamin K may be given IV, but IV administration carries a risk of anaphylactic-type reaction with little additional benefit. Fresh frozen plasma corrects coagulopathies more rapidly. Platelet transfusions may be needed for thrombocytopenia.
Drugs to reduce blood flow to the splanchnic bed: Administer a vasopressin IV drip (20 units in 200 mL NS) at 0.25 to 0.5 U/min to reduce blood flow in the splanchnic bed. Offset the potential coronary artery constriction associated with vasopressin with a nitroglycerine drip (25 mg in 250 mL NS) at 10 to 20 μg/min. Alternatively, Sandostatin (octreotide), a synthetic growth hormone, may be administered IV at 50 μg bolus over 3 minutes or diluted in 50 to 200 mL of NS and infused IV over 15 to 30 minutes. Additional 50 μg doses may be given hourly. This drug selectively limits splanchnic blood flow and thereby reduces portal hypertension. It is frequently effective in controlling esophageal variceal bleeding. Octreotide does not cause coronary artery constriction.
Obtain an ECG for signs of ischemia and treat according to ECG findings.
Insertion of an NG tube or large-bore orogastric tube to clear the stomach and monitor bleeding is a matter of judgment. The risk of stimulating more variceal bleeding somewhat offsets the advantages.
Emergency endoscopy, when available, with sclerosis of varices is the treatment of choice.
If bleeding continues in adults and emergency endoscopy with sclerosis of the varices is not available, consider the insertion of a Minnesota Tube as a temporizing measure. This is a large tube with both a gastric and an esophageal balloon. (Tracheal intubation may be needed prior to this procedure.) Insert the Minnesota tube through a bite block. Inflate the gastric balloon with 50 cc of air. Take an x-ray to be certain that the gastric balloon is in the stomach and not the esophagus. Then, inflate the gastric balloon to a volume of 350 cc. Pull the Minnesota tube through the bite block at a tension of about 2 lbs (the weight of a liter bag of NS) and secure it there with the sponge block that accompanies the tube. Attach suction to the esophageal and gastric ports. Irrigate the stomach and observe for continued bleeding from either port. If bleeding continues, fill the esophageal balloon to a pressure of 40 to 50 torr; observe again for bleeding. Determine and monitor balloon pressure by attaching a manometer to the system through one of the ports of a 3-way stopcock. (See illustration.) The Minnesota tube stops the esophageal bleeding about 60% to 70% of the time, but the patient with bleeding varices still needs to be seen by a specialist for an emergency consult for endoscopic treatment.
If these treatments do not stop bleeding, only emergency surgery or esophagoscopy with rubber band banding or sclerosis of varices will work.
Upper Gastrointestinal Bleeding, Stomach or Duodenum (Peptic
Ulcer/Gastritis)
A
history of epigastric pain and the absence of the stigmata of liver
disease make a bleeding peptic ulcer or gastritis likely in a patient
vomiting large amounts of blood. The amount of blood vomited with
bleeding ulcers is usually not as large as with bleeding varices,
because the blood tends to go down the gastrointestinal tract.
Initial Management
Airway Management: If the bleeding is severe, RSI (Vol II—Air Skills 4 Rapid Sequence Intubation) may be necessary. Perform as soon as intravenous routes are obtained.
Establish 2 large gauge IV lines.
Volume replacement: Begin a 1 to 2 liter saline bolus IV or (PEDS) a 10 to 20 mL/kg bolus in children. Begin blood infusion as soon as it becomes available to avoid hemodilution and hypocoagulopathy.
Insert a large bore orogastric tube and lavage with warm tap water. Observe for bleeding to clear.
Assess coagulation status: If the patient demonstrates a hypocoagulable state (bleeding from needle puncture sites, etc), assess (PT, PTT, platelet count, bleeding time, and clinical evidence of abnormal clotting) and treat coagulopathies induced by medications, disease states, or bleeding/ transfusions. Treatment may include Vitamin K 10 to 15 U IM or SQ. Vitamin K may be given IV, but IV administration carries a risk of anaphylactic-type reaction with little additional benefit. Fresh frozen plasma corrects coagulopathies more rapidly. Platelet transfusions may be needed for thrombocytopenia.
Suppression of gastric acid secretion: Medications such as H2 blockers (ranitidine [Zantac] 50 mg IV or famotidine [Pepcid] 20 mg IV) or protein-pump inhibitors (pantoprazole [Protonix] 80 mg IV followed by 8 mg/h by continuous drip) are choices to use as adjunctive treatments to suppress gastric secretion.
Drugs to reduce blood flow to the splanchnic bed may be considered: Administer a vasopressin IV drip (20 U in 200 mL NS) at 0.25 to 0.5 U/min to reduce blood flow in the splanchnic bed. Offset the potential coronary artery constriction associated with vasopressin with a nitroglycerine drip (25 mg in 250 mL NS) at 10 to 20 μg/min. Alternatively, Sandostatin (octreotide), a synthetic growth hormone, may be administered IV at 50 μg bolus over 3 minutes or diluted in 50 to 200 mL of normal saline and infused IV over 15 to 30 minutes. Additional 50 μg doses may be given hourly. This drug selectively limits splanchnic blood flow and thereby reduces portal hypertension. It is frequently effective in controlling esophageal variceal bleeding. Octreotide does not cause coronary artery constriction.
If bleeding continues, only emergency surgery or emergency gastroscopy with coagulation of bleeders will work.
For geriatric patients, obtain central venous access (Vol II—Circ Skills 2 Central Venous Access) to titrate volume resuscitation with central venous pressure. (Vol II—Circ Skills 3 Central Venous Pressure Measurement)
Rectal Bleeding
Bleeding from the upper GI tract
usually appears black or tarry (melanotic) at the rectum. However, if
the bleeding is brisk, it can appear bright red as with large bowel
bleeding (hematochezia).
Initial Management
Start IVs and administer a bolus of 1 to 2 liters of NS in adults and (PEDS:) a 10 to 20 mL/kg bolus in children. To avoid hemodilution and hypocoagulopathy, start blood replacement as soon as blood becomes available.
Insert a nasogastric tube to decompress the GI tract and to help localize the source of bleeding.
Assess coagulation status.
If bleeding continues, only emergency surgery or emergency endoscopy with coagulation will result in definitive treatment.
Bowel or Gastric Obstruction Present
Examine for abdominal distension with or without respiratory distress.
Initial Management
Establish intravenous fluid. While volume replacement with NS is the immediate concern, ongoing fluid and electrolyte losses may require potassium replacement and the use of D5 0.45 NS.
Insert a large orogastric tube for gastric and GI decompression. Consider pre-treating the nasal passage with topical anesthesia (lidocaine) and decongestant (phenylephrine) delivered by nasal spray. If the patient does not have a good gag reflex nor has a depressed LOC, orotracheally intubate (Vol II—Air Skills 3 Orotracheal Intubation) to avoid aspiration if the patient vomits.
If the abdominal distension disappears with gastric aspiration alone, there is probably gastric outlet obstruction. If the aspirate is fecal in appearance, there is probably a small or large bowel obstruction. Leave the gastric tube in place and periodically irrigate it to assure that it is draining the stomach.
Manage the airway carefully. Aspiration of feculent material is often a fatal complication of bowel obstruction.
Check the flat plate and upright x-rays of the abdomen for the typical appearance of sigmoid or cecal volvulus or air-fluid levels. If a volvulus is not seen on x-ray, the cause of the obstruction in adults could be adhesions from prior surgery, inflammation, or cancer. See numbers 12 and 13 in this pathway for management of a volvulus.
Leaking Abdominal Aortic Aneurysm
The
typical abdominal aortic aneurysm patient is in his or her sixties and
suffers an episode of syncope followed by abdominal, back, or flank
pain. Consider this diagnosis in any middle-aged or geriatric patient
in shock or with abdominal or back pain. Some patients feel an urge to
defecate: thus, they are often found in shock in the bathroom. If the
patient is awake, the abdomen will be tender as the examiner attempts
to feel for a pulsatile mass. If the patient is obese or severely
hypotensive, it is difficult to feel an aneurysm. A FAST exam with an
ultrasound probe can establish the presence of an aneurysm.
Alternatively, log roll the patient onto his or her side and shoot a
portable x-ray using lateral lumbar spine technique. This technique
causes the bowels to move out of the way, making the rim of calcium
outlining the aneurysm easier to see.
Initial Management
Administer oxygen and protect the airway.
Establish 2 large bore IVs and order type-specific blood.
Surgery is essential. Prepare the patient for surgery and obtain immediate surgical consultation.
Obtain an ECG.
Insert an oral gastric tube and a Foley catheter.
Blood and fluid replacement are in order, but attempt to maintain the systolic pressure at 90 to 100 torr as a goal.
Ruptured Ectopic Pregnancy
For
a woman of childbearing age in acute hypovolemic shock or with rapid
onset of severe lower abdominal pain, consider a diagnosis of ruptured
ectopic pregnancy. Consider ruptured ectopic pregnancy in every female
patient of childbearing age, unless circumstances (ie, prior
hysterectomy) rule it out. Note that while tubal ligation decreases the
overall incidence of pregnancy, it increases the proportion of
pregnancies that are ectopic. Severe lower abdominal pain is frequently
associated with the rupture; however, the patient may experience only a
vague discomfort or an urge to defecate. Besides performing a physical
examination, diagnostic tests include urine or serum pregnancy tests,
quantitative beta HCG, and serum progesterone. Blood count, blood type,
and blood for crossmatch may also be drawn. Urine pregnancy tests are
quite sensitive when the specific gravity is over 1.015, but serum
tests may be more convenient in an unstable patient. Serum progesterone
levels may also be useful in distinguishing early viable from
non-viable pregnancies, but cutoff values have ranged from 5 to 22
ng/mL in various studies.
In the acute setting, quantitative beta
HCGs are used in conjunction with ultrasound exam. With quantitative
beta HCG over 3000, if the pregnancy is intrauterine, an intrauterine
gestational sac should be seen with the vaginal probe. With
quantitative beta greater than 6000, gestational sac should be seen on
abdominal ultrasound. If an intrauterine gestational sac is seen, the
incidence of concurrent ectopic pregnancy is about 1 in 30 000. Note:
this rule does not apply in women undergoing infertility treatment, in
which multiple gestations are more common. If no gestational sac is
seen, this is consistent with ectopic pregnancy, even if no adnexal
mass is seen. Other ultrasound findings consistent with ruptured
ectopic include fluid in the cul de sac and in Morrison’s Pouch. If
ultrasound is unavailable, culdocentesis may be performed. Administer
mild analgesia as tolerated. Fill a syringe with 2 or 3 cc of local
anesthetic. Grasp the “wings” of a 19- or 21-gauge butterfly (scalp
vein) needle with a ring forceps and connect
the hub of the butterfly’s tubing to the syringe. Visualize the cervix
through the speculum opened wide. Grasp the cervix with a tenaculum and
lift up. Swab the posterior fornix with betadine. Use the butterfly
needle grasped by the ring forceps to infiltrate an area on the fornix,
and then puncture through this and aspirate with the syringe. (The
short length of the butterfly needle prevents penetration past the cul
de sac). Return of non-clotting blood is consistent with ruptured
ectopic, but a negative aspirate is meaningless. If a butterfly needle
is unavailable, some other type of needle/syringe may be used.
Initial Management
Establish 2 large bore IVs and begin saline infusion for volume replacement. Obtain blood for type and cross match. Use O negative if there is a delay.
Attempt to stabilize the patient with volume resuscitation, Trendelenburg positioning, and use of the PASG until surgical intervention is possible.
Arrange for immediate surgical consultation, even if the pregnancy test is negative. Whether the patient has a ruptured ectopic pregnancy, a ruptured ovarian cyst, or a spontaneous splenic rupture, a surgical emergency is in progress.
Administer RhoGAM to Rh-negative women. A dose of 50 μg is effective until 12 weeks of gestation due to the small volume of RBCs in the fetoplacental circulation, although there is no harm in giving the standard dose of 300 μg.1
Abdominal Viscus Perforation (Gastric Duodenal Ulcer, Appendix, or
Colonic Diverticulum)
Examine for signs of severe distress with a rigid abdominal wall that does not relax with ventilation. Lower lobe pneumonia can cause severe pain referred to the abdomen due to irritation of the diaphragms; however, the abdomen is not rigid and relaxes during exhalation.
Initial Management
If ruptured viscus is suspected, start an IV and insert a nasogastric tube.
Obtain an upright x-ray of the chest and look for free air under the diaphragm. Free air is not always seen even with perforation. If you suspect that a perforation has occurred from a gastric or duodenal ulcer, inject 100 cc of air through the nasogastric tube and take another x-ray. Insertion of gastrographin is another alternative to use to try to delineate the presence of a ruptured gastric or duodenal ulcer. CT, if available, should also show free air; but if a perforation is suspected, initially avoid the use of barium contrast by performing a non-contrast CT.
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If a ruptured gastric or duodenal ulcer is demonstrated, administer third-generation cephalosporin, such as ceftriaxone (Rocephin) 2 g IV. PEDS: In children, administer ceftriaxone 50 mg/kg (up to 2 g) IV. If some other viscus is the likely source of rupture, see Vol III—IN4 Abdominal Sepsis for recommendations of IV antibiotics.
Surgery is required to over-sew the perforation and to lavage the abdominal cavity.
Abdominal Sepsis/Peritonitis
Abdominal
sepsis with peritonitis is usually accompanied by marked abdominal
pain, abdominal distension, or sometimes a palpable mass. Typical signs
of peritonitis are usually present including a tender abdomen with
guarding, rigidity, and/or percussion tenderness. Temperature elevation
is frequently present. Bowel sounds may or may not be present
initially. Geriatric patients and (PEDS:) small children may show few
signs of abdominal sepsis. Conduct a careful abdominal examination of
any patient in septic shock. Repeat the exam as necessary. A rectal
examination may reveal a mass or localized tenderness. Ruptured viscus
may be diagnosed by the presence of free air on upright abdominal or
chest x-ray (see #8 this pathway). Pancreatitis, diverticulitis with
sepsis and/or perforation, ascending cholangitis, peri-renal or psoas
abscess, embolization of splanchnic arteries, arteriosclerosis with
bowel infarction, peritoneal dialysis, or primary spontaneous bacteria
peritonitis are some of the many causes of abdominal sepsis.
Initial Management
Monitor vital signs, ECG, and oxygen saturation carefully. Obtain blood gases to detect lactic acidosis.
Treat septic shock with a 1 to 2 liter bolus of NS in adults or (PEDS:) a 10 to 20 mL/kg in children.
If large volumes are needed, switch to Ringer’s lactate solution to avoid hyperchloremic acidosis.
In older adults, obtain central venous access (Vol II—Circ Skills 2 Central Venous Access) to measure central venous pressure (Vol II—Circ Skills 3 Central Venous Pressure Measurement) to titrate further volume replacement.
Broad-spectrum antibiotics are necessary. (Vol III—IN3 Sepsis in Adults, IN4 Abdominal Sepsis)
Do not resort to vasopressor treatment of shock, unless blood volume is restored and hypotension persists.
Intussusception
PEDS:
Ileocolic intussusception occurs most commonly in the 3-month to 3-year
age group. The ileum inverts on itself and pushes distally into the
cecum where it becomes edematous, friable, and bloody. Commonly the
child has a history of recurrent unexplained bouts of abdominal pain.
There may be a history of bloody, mucous-covered stool. This has been
called “currant jelly” stool. On physical examination, it may be
possible to palpate a thickened and tender cecum. An abdominal x-ray
may reveal thickened rings of the distal ilium with proximal
obstruction, but these findings are not always present. In younger
children, the diagnosis can be difficult. In young infants or in late
stages, intussusception may present as lethargy, vomiting, poor
feeding, or shock.
Initial Management
The treatment is an emergent barium or air enema that pushes the ileum back out of the cecum. This is successful in reducing the intussusception about 80% of the time.
If unsuccessful, surgery is needed.
Severe Dehydration in Small Children Secondary to Vomiting and Diarrhea
PEDS:
Severe dehydration can be a life-threatening emergency. The child may
have a depressed level of consciousness and be unable to feed or eat.
Initial Management
Obtain IV access and administer a bolus of saline 20 mL/kg. Reassess for hypovolemia. Hypoglycemia, lactic acidosis, and electrolyte abnormalities may be found. Aggressive restoration of blood volume is the most important action.
Antibiotics should be considered in children < 6 months because of a high incidence of bacteremia in this age group. In older children, antibiotics may also be indicated when the diarrhea has been present for 10 to 14 days.
Obtain stool and blood cultures before instituting antibiotic therapy. Most cases turn out to be viral, but this is difficult to ascertain initially.
Volvulus in Infants and Children
PEDS:
In children, volvulus usually involves the cecum and the distal small
bowel. The amount of bowel involved varies considerably. It is caused
by a failure of the ascending colon and cecum to attach to the
posterior abdomen allowing the hypermobile cecum and distal ileum to
rotate around the mesenteric pedicle of the ileocecal artery, producing
a closed-loop obstruction and a strangulation of the bowel. This can be
difficult to diagnose. Bilious vomiting secondary to small bowel
obstruction is a clue. If not corrected early, this can lead to septic
shock. Abdominal x-rays are rarely diagnostic, but classical findings
include a dilated bowel segment. Barium enema may demonstrate the
“bird’s beak” characteristic of volvulus.
Initial Management
Intravenous therapy is necessary.
Surgical intervention is needed. Obtain surgical consult.
Volvulus in Adults
Volvulus
is torsion of a segment of the alimentary tract that usually leads to a
bowel obstruction. The most common locations for volvulus in adults are
the cecum and the sigmoid colon. Other potential locations that may
form a volvulus include the transverse colon, splenic flexure of the
colon, or a segment of the small bowel. Most patients complain of
symptoms similar to a bowel obstruction with nausea, vomiting,
abdominal pain, and constipation. Physical examination discloses a
distended abdomen representing dilated loops of colon and small bowel.
Abdominal x-rays commonly show distended loops of small bowel with a
large air-filled loop of colon. CT scan or contrast enema may be
diagnostic, but do not perform contrast enema in patients if intestinal
gangrene is suspected. The characteristic contrast enema finding of a
colon volvulus is the “bird’s beak.”
Initial Management
Intravenous hydration is necessary.
A nasogastric or orogastric tube is necessary to avoid gastric distension and subsequent regurgitation and aspiration.
Early surgical consultation is needed.
In some cases, decompression can be achieved with a rectal tube advanced into an obstructed loop of sigmoid colon under direct vision with a colonoscope.
A dilated volvulus (measuring 12 cm across) is in danger of losing its blood supply; perforation is imminent.
Acute Mesenteric Ischemia
Acute
mesenteric ischemia typically presents as severe but diffuse abdominal
pain with minimal tenderness on physical examination. Patients may
report recent similar postprandial pain. In about half of cases, occult
blood may be present in the stool. As ischemia progresses, the bowel
may perforate and produce more classic peritonitis. Combined with the
frequent co-morbidities in the patient group, a mortality rate >
70%
is expected once the bowel is infarcted. To prevent this outcome,
maintain a high index of suspicion and pursue the diagnosis
aggressively. While no simple lab test is diagnostic, a persistently
normal serum lactate is helpful in excluding the diagnosis, but the
test must be repeated over time to help confirm a negative impression.
Definitive diagnosis is by angiography or Gadolinium-enhanced MRA
(magnetic resonance angiogram).
Initial Management
Hydration via IV is needed as part of the initial stabilization.
Angiographic infusion of papaverine may be effective in patients who do not have bowel tissue necrosis.
Surgical consultation is frequently required.
Cholangitis
Cholangitis
is another potentially life-threatening condition most commonly
observed in geriatric or AIDS patients. In addition to the usual signs
and symptoms of biliary disease, the patient may be febrile, shocky,
and have an altered mental status. At times, these manifestations may
overshadow the biliary pain. Elevated WBC count, bilirubin, and liver
function tests are consistent with this diagnosis. Ultrasound may
confirm gallstones and a dilated ductal system. CT may also be useful.
Nuclear studies, such as HIDA scanning (cholescintigraphy), are
sensitive for early obstruction.
Initial Management
Hydration via IV is needed as part of initial stabilization.
Antibiotics need to be initiated early. Recommended antibiotic regimens include ampicillin/sulbactam 3 g IV or ceftriaxone 2 g plus metronidazole 1 g IV.
Endoscopic retrograde cholangiopancreatography (ERCP), if available, may be both diagnostic and therapeutic.
Surgical consultation is often needed.
Caveats
Suspect a leaking abdominal aneurysm in any middle-aged or geriatric patient in shock.
Digitalis toxicity is usually exhibited as a rhythm problem, but prominent gastrointestinal symptoms may be present.
Ischemic bowel can result from embolism, arteriosclerosis, venous thrombosis, or strangulation from a volvulus or internal hernia.
A dilated volvulus (measuring 12 cm across) is in danger of losing its blood supply; perforation is imminent.
Gastric decompression in bowel obstruction saves lives by preventing vomiting and aspiration.
Keys to resuscitation are good airway management (Vol II—Air Skills Portals) and good blood volume management. (Vol III—Trau Care 2 Shock)
References
Physicians’ Desk Reference 2003 (57th edition). Medical Economics Company (November 2002).
- Prevention of Rho (D) alloimmunization. American College of Obstetricians and Gynecologists Practice Bulletin No 4. American College of Obstetricians and Gynecologists, Washington.