ADULT HEALTH NURSING PHASE I

Thursday 6:00-9:00 pm

Submitted by:
LAVINIA S. MALAZARTE

IRRITABLE BOWEL SYNDROME

 • A functional disorder of the motility of the intestines
• No organic disease or anatomic abnormality
• Occurs more common in women than in
Related factors:
Heredity
Psychological stress
Illness
Diet high in irritating foods
Alcohol consumption
Smoking

PATHOPHYSIOLOGY

• Results from a functional disorder of intestinal motility. This may be related to:
- Neurologic regulatory system
- Infection or irritation
- Vascular or metabolic disturbance
• Peristaltic waves are affected at different segments of the intestine and in the intensity with which they propel the fecal
matter forward

Assessment:
 Primary symptom is alteration in bowel patterns – constipation, diarrhea, or a combination of both
 Often accompanied by pain, bloating, abdominal distention,
 Abdominal pain is often precipitated by eating and is often relieved by defecation

Diagnostic Exams:
o Barium Enema
 May reveal spasm, distention, and/or mucus accumulation in the intestine
o Manometry and electromyography
 Study interluminal pressure changes generated by spaticity
o Stool studies, contrast x-ray studies, protoscopy
 Rules out other colon diseases

Medical Mangement
• Goals of treatment:
 Relieve abdominal pain
 Control diarrhea and/or constipation
 Reduce stress
• Avoid irritants (beans, caffeinated products, fried foods, alcohol, spicy foods)
• A well-balanced, high fiber diet is prescribed to hlp control diarrhea and constipation
• Exercise can assist in reducing anxiety and increasing intestinal motility
• Hydrophilic colloids (bulk) and antidiarrheal agents maybe given to control the diarrhea and fecal urgency.
• Antidepressants can assist in treating underlying anxiety and depression
• Anticholinergics and calcium channel blockers decrease smooth muscle spasm, decreasing cramping and constipation

Nursing Management:
 Provide patient and family education
o Emphasis is placed on teaching and reinforcing food dietary habits
o Patient is encouraged to eat at regular times and chew food thoroughly
o Patient should understand although adequate fluid is intake is necessary, fluid should not be taken with meals to avoid
abdominal distention.
o Alcohol use and cigarette smoking is discouraged

HEPATIC FAILURE
 is a condition in which the rapid deterioration of liver function results in coagulopathy and alteration in the mental status of
a previously healthy individual.
 The term acute liver failure is used to describe the development of coagulopathy, usually an international normalized ratio
(INR) of greater than 1.5, and any degree of mental alteration (encephalopathy) in a patient without preexisting cirrhosis and
with an illness of less than 26 weeks' duration.
 According to time-length between first signs of liver disease and development of encephalopathy:
 Fulminant: acute liver disease with encephalopathy within 8 weeks of first sign of liver disease.
 Acute: up to 28 days
 Subacute:5-12 weeks
 Drug-related hepatotoxicity is the leading cause of acute liver failure
 Despite aggressive treatment, many patients die from fulminant hepatic failure.
 Before orthotopic liver transplantation (OLT),for fulminant hepatic failure, the mortality rate was generally greater than
80%.
 Approximately 6% of OLTs performed in the United States are for fulminant hepatic failure. However, with improved
intensive care, the prognosis is much better now than in the past, with some series reporting approximately a survival rate of
60%.

Pathophysiology

• acetaminophen overdose
• idiosyncratic drug reaction
• viral hepatitis
• ingestion of amanita falloides maushroom
• Wilson’s disesase
• Reye’ syndrome
• HELLP syndrome
• malignancies

↓
↑ ammonia levels ↑ nitric oxide levels
↓ ↓
impaired osmoregulation in the brain vasodilation
↓ ↓
cerebral edema ↔ ICH ← ↑cerebral blood flow
↓ ↓
neurological damage circulatory insufiiciency & poor organ perfusion
↓ ↓
brain death multisystem organ failure
↓
DEATH
Clinical Manifestations:
All patients with clinical or laboratory evidence of moderate or severe acute hepatitis should have immediate measurement of
prothrombin time (PT) and careful evaluation of mental status. The patients should be admitted to the hospital if there is
alteration in mental sensorium or prothrombin time is prolonged.
• The patient history is valuable for guiding appropriate interventions.
o If the patient is incapacitated, closely question family members and friends.
o Detail the date of onset of jaundice and encephalopathy, alcohol use, medication use (prescription and illicit or
recreational), herbal or traditional medicine use, family history of liver disease (Wilson disease), exposure risk factors for viral
hepatitis (travel, transfusions, sexual contacts, occupation, body piercing), and toxin ingestion (mushrooms, organic solvents,
phosphorus contained in fireworks).
o Determine if any complications have developed.
Assessment
• Jaundice is often but not always present.
• Right upper quadrant tenderness is variably present.
• An enlarged liver may be seen with congestive heart failure, viral hepatitis, or Budd-Chiari syndrome.
• Development of cerebral edema ultimately may give rise to manifestations of increased intracranial pressure (ICP),
including papilledema, hypertension, and bradycardia.
• The rapid development of ascites, especially if observed in a patient with fulminant hepatic failure accompanied by
abdominal pain, suggests the possibility of hepatic vein thrombosis (Budd-Chiari syndrome).
• Hematemesis or melena may complicate the presentation of fulminant hepatic failure as a result of upper gastrointestinal
(GI) bleeding.
• Typically, patients are hypotensive and tachycardic as a result of the reduced systemic vascular resistance that
accompanies fulminant hepatic failure, a pattern that is indistinguishable from septic shock.
Laboratory Studies
• Complete blood cell (CBC) count: Results may indicate thrombocytopenia.
• PT and/or international normalized ratio (INR)
o These tests are used to determine the presence or severity of coagulopathy.
o They are sensitive markers of hepatic synthetic failure but rarely in the setting of suspected fulminant hepatic failure.
• Hepatic enzymes
o Levels of the transaminases (aspartate aminotransferase [AST]/serum glutamic-oxaloacetic transaminase [SGOT] and
alanine aminotransferase [ALT]/serum glutamic-pyruvic transaminase [SGPT]) are often elevated dramatically as a result of
severe hepatocellular necrosis.
o In instances of acetaminophen toxicity (especially alcohol-enhanced), the AST level may be well over 10,000 U/L.
o The alkaline phosphatase (ALP) level may be normal or elevated.
• Serum bilirubin
o By definition, this value should be elevated in fulminant hepatic failure. It climbs as hepatic dysfunction worsens.
o Serum bilirubin that is elevated greater than 4 mg/dL suggests a poor prognosis in the setting of acetaminophen poisoning.
• Serum ammonia
o This level may be elevated dramatically in patients with fulminant hepatic failure. Arterial blood is the best way to measure
ammonia.
o The arterial serum ammonia level is most accurate, but venous ammonia levels are generally acceptable.
o It does not exclude the possibility of another cause for mental status changes (notably increased ICP and seizures).
• Serum glucose: levels may be very low and pose a serious hazard. This results from impairments in glycogen production.
• Serum lactate
o Arterial blood lactate levels either at 4 hours (>3.5 mmol/L) or at 12 hours (>3.0 mmol/L) are early predictors of outcome
in acetaminophen-induced acute liver failure. levels are often elevated as a result of both impaired tissue perfusion (increases
production) and decreased clearance by the liver.
o An increased anion gap metabolic acidosis is associated with this condition (although it may be accompanied by a
respiratory alkalosis as a result of hyperventilation).
• Arterial blood gases (ABGs): These may reveal hypoxemia, which is a significant concern as a result of adult respiratory
distress syndrome (ARDS) or other causes (eg, pneumonia).
• Serum creatinine: levels may be elevated, signifying the development of hepatorenal syndrome or some other cause of
acute renal failure.
• Blood cultures
o Most patients develop some sort of infection during or before hospitalization. Patients are at risk of line sepsis and
complications from all other invasive procedures.
o Fungal infections are common, most likely as a result of decreased host resistance and antibiotic treatment.
o Infection may be associated with bacteremia, but identifying and treating it early is important because the mortality from
fulminant hepatic failure increases significantly with the development of this serious complication.
• Serum-free copper
o Serum-free copper studies are important to consider when Wilson disease must be excluded or confirmed. Fulminant
hepatic failure from Wilson disease appears to be uniformly fatal without transplantation.
• Serum phosphate
o Levels of serum phosphate may be low.
o It has been hypothesized that people whose livers rapidly regenerate will develop hypophosphatemia. Elevated phosphate
levels suggest impaired regeneration.
• Viral serologies
o HAV immunoglobulin M (IgM), hepatitis B surface antigen (HBsAg), and HBV anticore IgM serologies help determine acute
infection with HAV or HBV.
• Autoimmune markers: Antinuclear antibody (ANA), anti-smooth muscle antibody (ASMA), and immunoglobulin levels are
important markers for a diagnosis of autoimmune hepatitis.
• Acetaminophen level
o The acetaminophen level may have decreased by the time a patient presents with fulminant hepatic failure, but it may be
helpful for documentation purposes.
• Drug screen: Consider a drug screen in a person who is an IV drug abuser.
Imaging Studies
• Liver ultrasonography (Doppler)
o This examination may establish the patency and flow in the hepatic vein (allowing exclusion of Budd-Chiari syndrome),
hepatic artery, and the portal vein.
o Liver ultrasonography establishes the presence of ascites.
• Computed tomography (CT) scanning or magnetic resonance imaging (MRI) of the abdomen
o These may be required for further definition of hepatic anatomy and to help the clinician exclude other intraabdominal
processes, particularly if the patient has developed massive ascites, is obese, or if transplantation is being planned .
o Intravenous contrast may compromise renal function. Consider performing a contrast-free study.
• CT scanning of the head helps identify cerebral edema and exclude intracranial mass lesions (especially hematomas) that
may mimic edema from fulminant hepatic failure. Also consider and exclude subdural hematomas (see image below).
Procedures
• Liver biopsy:
o A percutaneous liver biopsy is contraindicated in the setting of coagulopathy. However, a transjugular biopsy is helpful for
diagnosis if autoimmune hepatitis, metastatic liver disease, lymphoma, or herpes simplex hepatitis is suspected.
• Intracranial pressure monitoring
o When establishing a diagnosis of ICH or cerebral edema, this approach is frequently necessary and has value in guiding
management.
o Typically, extradural catheters are safer than intradural catheters. Intradural catheters are somewhat more accurate and,
in the hands of a neurosurgeon experienced with their use, may be equally safe.
Management
• The most important step is to identify the cause of liver failure.
• It is also critical to identify those patients who will be candidates for liver transplantation.
• The most important aspect of treatment in patients with acute liver failure is to provide good intensive care support.
Patients with grade II encephalopathy should be transferred to the intensive care unit (ICU) for monitoring.
• Most patients with acute liver failure tend to develop some degree of circulatory dysfunction. Careful attention should be
paid to fluid management, hemodynamics, metabolic parameters, and surveillance of infection.
• Maintenance of nutrition and prompt recognition of gastrointestinal bleeding are crucial. Coagulation parameters, CBC
count, and metabolic panel should be checked frequently. Serum aminotransferases and bilirubin are generally measured daily to
follow the course of infection. Intensive care management includes recognition and management of complications.
• As the patient develops progressive encephalopathy, protection of the airway is important.
• Airway protection
o As the patients with fulminant hepatic failure drift deeper into coma, their ability to protect their airway from aspiration
decreases. Patients who are in stage III coma should have a nasogastric tube (NGT) for stomach decompression. When patients
progress to stage III coma, intubation should be performed.
o Short-acting benzodiazepines in low doses (eg, midazolam 2-3 mg) may be used before intubation or propofol (50
mcg/kg/min) may be initiated before intubation and continued as an infusion. Propofol is also known to decrease the cerebral
blood flow and ICH. It may be advisable to use endotracheal lidocaine before endotracheal suctioning.
• Encephalopathy and cerebral edema
o Patients with grade I encephalopathy may sometimes be safely managed on a medical ward. Frequent mental status
checks should be performed with transfer to an ICU warranted with progression to grade II encephalopathy.
o Head imaging with CT scanning is used to exclude other causes of decline in mental status, such as intracranial
hemorrhage.
o Sedation should be avoided if possible; unmanageable agitation may be treated with short-acting benzodiazepines in low
doses.
o Patients should be positioned with the head elevated at 30°.
o Efforts should be made to avoid patient stimulation. Maneuvers that cause straining or, in particular, Valsalva-like
movements may increase ICP.
o There is increasing evidence that ammonia may play a pathogenic role in the development of cerebral edema. Reducing
elevated ammonia levels with enteral administration of lactulose might help prevent or treat cerebral edema.
o ICP monitoring helps in the early recognition of cerebral edema. The clinical signs of elevated ICP, including hypertension,
bradycardia, and irregular respirations (Cushing triad), are not uniformly present; these and other neurologic changes, such as
pupillary dilatation or signs of decerebration, are typically evident only late in the course.
o The ultimate goal of such measures is to maintain neurologic integrity and prolong survival while awaiting receipt of a
donor organ or recovery of sufficient functioning hepatocyte mass.
• Cardiovascular monitoring
o Homodynamic derangements consistent with multiple organ failure occur in acute liver failure. Hypotension (systolic, <80
mm Hg) may be present in 15% of patients.
o Most patients will require fluid resuscitation on admission. Intravascular volume deficits may be present on admission due
to decreased oral intake or gastrointestinal blood loss. Hemodynamic derangement resembles that of sepsis or cirrhosis with
hepatorenal syndrome (low SVR with normal or increased cardiac output). An arterial line should be placed for continuous blood
pressure monitoring.
o A Swan–Ganz catheter should be placed and fluid replacement with colloid albumin should be guided by the filling
pressure. If needed, dopamine or norepinephrine can be used to correct hypotension.
• Management of coagulopathy
o In the absence of bleeding, it is not necessary to correct clotting abnormalities with fresh frozen plasma (FFP); the
exception is when an invasive procedure is planned or in the presence of profound coagulopathy.
o Recombinant factor VIIa may be used in patients whose condition is nonresponsive to FFP
o Platelet transfusions are not used until the count is less than 10,000/µL or if an invasive procedure is being done and the
platelet count is less than 50,000/µL.
• Managing poisonings (eg, acetaminophen, mushroom) requires specific treatment distinct from other, more general issues
related to fulminant hepatic failure.
o Treat acetaminophen (paracetamol, APAP) overdose with N-acetylcysteine (NAC).
o A phalloides mushroom intoxication is much more common in Europe as well as in California. Treat with IV penicillin G,
even though its mode of action is unclear. Silibinin, a water-soluble derivative of silymarin, may be administered orally, and oral
charcoal may be helpful by binding the mushroom toxin.
Surgical Care
Liver transplantation is the definitive treatment in liver failure.

Diet
• Patients with acute liver failure are, by necessity, nothing by mouth (NPO). They may require large amounts of IV glucose
to avoid hypoglycemia.
• When enteral feeding via a feeding tube is not feasible (eg, as in a patient with paralytic ileus), institute total parenteral
nutrition (TPN).
• Restricting protein (amino acids) to 0.6 g/kg body weight per day was previously routine in the setting of hepatic
encephalopathy, but this may not be necessary.
Activity
Bedrest is recommended.
Medication
• Multiple medications may be necessary in patients with acute liver failure because of the wide variety of complications that
may develop from fulminant hepatic failure. Decreased hepatic metabolism and the potential for hepatotoxicity become central
issues.
• Antidotes that effectively bind or eliminate A phalloides toxin and toxic metabolites of acetaminophen are essential.
• Acetaminophen ingestion of more than 10 g may be hepatotoxic due to formation of a highly reactive toxic intermediate
metabolite, which is ordinarily metabolized further in the presence of glutathione to N -acetyl-p-aminophenol-mercaptopurine.
• Administering NAC permits restitution of intrahepatic glutathione. NAC is most effective when administered within 12-20
hours following acetaminophen overdose.
• Never administer aminoglycosides and NSAIDs, because the potential for nephrotoxicity is exaggerated greatly in this
setting.
Antidotes
Antidotes neutralize toxic agents.
Penicillin G (Pfizerpen)
First DOC. Treatment of Amanita poisoning is with IV penicillin G, although mode of action is unclear.
Silibinin (Silibinin Plus)
Water-soluble derivative of silymarin, which is the active ingredient in herbal preparation milk thistle. Possesses antioxidant
properties that may benefit liver disease management.
Activated charcoal (Actidose-Aqua, Liqui-Char, CharcoAid)
If ingestion has been recent, Amanita toxin may be bound to charcoal and absorption prevented.
N-acetylcysteine (Mucomyst, Mucosil)
First DOC in acetaminophen overdose. Provides reducing equivalents to help restore depleted intrahepatic glutathione levels.
Complications
• Hepatic encephalopathy
• Manage hepatic encephalopathy in the conventional way, by providing lactulose and avoiding sedatives. In the late stages
of encephalopathy, avoid providing lactulose by mouth or nasogastric tube without previous intubation, considering the risk of
aspiration.
• Hepatic encephalopathy is not truly a complication because it is required for the diagnosis of fulminant hepatic failure, but
evolution to higher stages of hepatic encephalopathy may result in patients losing their abilities to maintain their airways.
• Cerebral edema
• The occurrence of cerebral edema and ICH in patients with acute liver failure is related to the severity of encephalopathy.
Cerebral edema is seldom observed in patients with grades I-II encephalopathy. The risk of edema increases to 25-35% with
progression to grade III and to 65-75% (or more) in patients reaching grade IV coma.
• Patients in the advanced stages of encephalopathy require close follow-up care. Monitoring and management of
hemodynamic and renal parameters, as well as glucose, electrolytes, and acid/base status, become critical. Frequent neurologic
evaluation for signs of elevated ICP should be conducted.
• ICP monitoring
• ICP monitoring helps in the early recognition of cerebral edema. The clinical signs of elevated ICP, including hypertension,
bradycardia, and irregular respirations (Cushing triad), are not uniformly present; these and other neurologic changes, such as
papillary dilatation or signs of decerebration, are typically evident only late in the course.
• CT scanning of the brain does not reliably demonstrate evidence of edema, especially in the early stages. A primary
purpose of ICP monitoring is to detect elevations in ICP and reductions in CPP, so that interventions can be made to prevent
herniation while preserving brain perfusion.
• The ultimate goal of such measures is to maintain neurologic integrity and to prolong survival while awaiting receipt of a
donor organ or recovery of sufficient functioning hepatocyte mass.
• Correct coagulopathy and bleeding tendencies with the use of FFP and platelet infusion.
• If an ICP monitor is placed, ICP should be maintained below 20-25 mm Hg, if possible, with CPP maintained above 50-60
mm Hg. Support of systemic blood pressure may be required to maintain adequate CPP.
• ICH
• is managed initially by the use of mannitol. Osmotic diuresis with IV mannitol is effective in the short term in decreasing
cerebral edema.
• Administration of IV mannitol (in a bolus dose of 0.5-1 g/kg or 50-100 g) is recommended to treat ICH in acute liver failure.
• Other measures can be used to treat ICH.
• Hyperventilation may be instituted temporarily in an attempt to acutely lower ICP and to prevent impending herniation
• Hyperventilation to reduce the partial pressure of carbon dioxide in the blood (PaCO2) to 25-30 mm Hg is known to quickly
lower ICP via vasoconstriction, causing decreased cerebral blood flow, but this effect is short-lived.
• Seizures, which may be seen as a manifestation of the process that leads to hepatic coma and ICH, should be controlled
with phenytoin
• Hemorrhage
o This develops as a result of the profoundly impaired coagulation that manifests in these patients.
o Correct coagulopathy, as earlier outlined.
o The transfusion requirements for coagulation products (FFP, platelets) may be enormous. Multiple transfusions with packed
red blood cells may be needed.
o Gastrointestinal bleeding may develop from esophageal, gastric, or ectopic varices as a result of portal hypertension.
Portal hypertensive gastropathy and stress gastritis may also develop.
• Infection prophylaxis and treatment
o Periodic surveillance cultures should be performed to detect bacterial and fungal infections.
o In hospital-acquired IV catheter infections, consider vancomycin.
• Renal electrolyte and acid-base imbalances
o Acute renal failure is a frequent complication in patients with acute liver failure and may be due to dehydration,
hepatorenal syndrome, or acute tubular necrosis.
o Maintain adequate blood pressure, avoid nephrotoxic medications and NSAIDs, and promptly treat infections.
o When dialysis is needed, continuous (ie, continuous venovenous hemodialysis [CVVHD]) rather than intermittent renal
replacement therapy is preferred.
• Metabolic concerns
o Alkalosis and acidosis occur; identify and treat the underlying cause.
o Base deficits can be corrected by THAM solution (tromethamine injection), which prevents a rise in carbon dioxide,
osmolality, and serum sodium.
o Severe hypoglycemia occurs in approximately 40% of patients with fulminant hepatic failure. Although hypoglycemia
occurs more frequently in children, it needs to be monitored in adult patients as well.
o Blood sugars should be maintained in the range of 60-200 mg/dL with the infusion. Use 10% dextrose solution and glucose
monitoring.
o Phosphate, magnesium, and potassium levels are low and require frequent supplementation.

ABDOMINAL TRAUMA

• Blunt Abdominal Trauma

Blunt abdominal trauma usually results from motor vehicle collisions, assaults, recreational accidents, or falls. The most
commonly injured organs are the spleen, liver, retroperitoneum, small bowel, kidneys (see image below), bladder, colorectum,
diaphragm, and pancreas. Men tend to be affected slightly more often than women.

Pathophysiology
• Vehicular trauma is by far the leading cause of blunt abdominal trauma in the civilian population. Auto-to-auto and auto-to-
pedestrian collisions have been cited as causes in 50-75% of cases.
• Rare causes of blunt abdominal injuries include iatrogenic trauma during cardiopulmonary resuscitation, manual thrusts to
clear an airway, and the Heimlich maneuver.
• Intra-abdominal injuries secondary to blunt force are attributed to collisions between the injured person and the external
environment and to acceleration or deceleration forces acting on the person's internal organs.
• Blunt force injuries to the abdomen can generally be explained by 3 mechanisms:
o The first is when rapid deceleration causes differential movement among adjacent structures. As a result, shear forces are
created and cause hollow, solid, visceral organs and vascular pedicles to tear, especially at relatively fixed points of attachment
o The second is when intra-abdominal contents are crushed between the anterior abdominal wall and the vertebral column
or posterior thoracic cage. This produces a crushing effect, to which solid viscera (eg, spleen, liver, kidneys) are especially
vulnerable.
o The third is external compression forces that result in a sudden and dramatic rise in intra-abdominal pressure and
culminate in rupture of a hollow viscous organ.
Assessment
The initial assessment of a trauma patient begins at the scene of the injury, with information provided by the patient, family,
bystanders, or paramedics.
The most reliable signs and symptoms in alert patients are :
o pain
o tenderness
o gastrointestinal hemorrhage
o hypovolemia
o Seat belt sign
o Abdominal distention
o Retroperitoneal hemorrhage:
o Grey Turner sign - ecchymosis involving the flanks
o Cullen sign - ecchymosis involving the umbilicus
o Auscultation of bowel sounds in the thorax may indicate the presence of a diaphragmatic injury.
o Palpation may reveal local or generalized tenderness, guarding, rigidity, or rebound tenderness, which suggests peritoneal
injury.
o A rectal examination should be performed to search for evidence of bony penetration resulting from a pelvic fracture
o Stool should be evaluated for gross or occult blood.

Laboratory Studies
• CBC count, coagulation studies, blood type, and blood cross-match (if indicated). The presence of massive hemorrhage is
usually obvious from hemodynamic parameters, and the hematocrit value merely confirms the diagnosis.
• Urine studies include urinalysis, urine toxicologic screen, and serum or urine pregnancy tests in females of appropriate
age.
• Amylase or lipase levels may be elevated because of pancreatic ischemia caused by the systemic hypotension that
accompanies trauma.
Imaging Studies
• Plain radiograph
o The chest radiograph may aid in the diagnosis of abdominal injuries such as ruptured hemidiaphragm (eg, a nasogastric
tube seen in the chest) or pneumoperitoneum.
o The pelvic or chest radiograph can demonstrate fractures of the thoracolumbar spine.
o The presence of transverse fractures of the vertebral bodies, ie, Chance fractures, suggests a higher likelihood of blunt
injuries to the bowel.
o In addition, free intraperitoneal air, or trapped retroperitoneal air from duodenal perforation, may be seen.
• Ultrasound
o procedure of choice in the evaluation of hemodynamically unstable trauma patients.
o An examination is interpreted as positive if fluid is found in any of the 4 acoustic windows and is interpreted as negative if
no fluid is seen. An examination is deemed indeterminate if any of the windows cannot be adequately assessed.
• Computed tomography
o The CT scan remains the criterion standard for the detection of solid organ injuries.
o CT scans, have the capability to determine the source of hemorrhage, as shown below.
Other Tests
• Laparoscopy
o Diagnostic laparoscopy has been most useful in the evaluation of possible diaphragmatic injuries, especially in penetrating
thoracoabdominal injuries on the left side.
Diagnostic Procedures
• Diagnostic peritoneal lavage
o the sampling of peritoneal fluid in cases of acute pancreatitis and blunt abdominal trauma by passing a spinal needle
through the abdominal wall.
o DPL is indicated in blunt trauma in
(1) patients with a spinal cord injury,
(2) those with multiple injuries and unexplained shock,
(3) obtunded patients with a possible abdominal injury,
(4) intoxicated patients in whom abdominal injury is suggested
(5) patients with potential intra-abdominal injury who will undergo prolonged anesthesia for another procedure.
o The only absolute contraindication to DPL is the obvious need for laparotomy. Relative contraindications include morbid
obesity, a history of multiple abdominal surgeries, and pregnancy.
Management
o The initial goal is to rapidly assess the patient's airway with cervical spine precautions, breathing, and circulation. This is
then followed by splinting of fractures and control of external hemorrhage.
o The injured patient is at risk for progressive deterioration from continued bleeding and requires rapid transport to a trauma
center.
o The next priority in the primary survey is an assessment of the circulatory status of the patient. Circulatory collapse in a
patient with blunt abdominal trauma is usually caused by hypovolemia from hemorrhage.
o Angiography is a valuable modality in the nonoperative management of adult abdominal solid organ injuries from blunt
trauma. It is used aggressively for nonoperative control of hemorrhage, thus avoiding nontherapeutic cost-inefficient
laparotomies.
Surgical Management
o Resuscitative thoracotomy in the emergency department is only occasionally life-saving. It is an aggressive, desperate
measure to save a patient in whom death is thought to be imminent or otherwise inevitable.
o In a patient with hemoperitoneum from blunt thoracoabdominal trauma, the purpose of a resuscitative thoracotomy in the
emergency department is to (1) cross-clamp the aorta, diverting available blood to the coronaries and cerebral vessels during
resuscitation; (2) evacuate pericardial tamponade; (3) directly control thoracic hemorrhage; and (4) open the chest for cardiac
massage.
o Laparotomy
o hemorrhage control is accomplished by removing blood and clots, packing all 4 quadrants, and clamping vascular
structures. Obvious hollow viscus injuries are sutured. After intra-abdominal injuries have been repaired and hemorrhage has
been controlled by packing, a thorough exploration of the abdomen is then performed to evaluate the entire contents of the
abdomen.
II. Penetrating abdominal trauma
o implies that either a GSW or a stab wound has violated the abdominal cavity.
Pathophysiology
o A GSW is caused by a missile propelled by combustion of powder. These wounds involve high-energy transfer and,
consequently, can have an unpredictable pattern of injuries.
o Secondary missiles, such as bullet and bone fragments, can inflict additional damage. Military and hunting firearms have
higher missile velocity than handguns, resulting in even higher energy transfer. Close-range shotgun injuries often cause
significant tissue damage and should be considered high-energy transfer injuries as well.
o Stab wounds are caused by penetration of the abdominal wall by a sharp object. This type of wound generally has a more
predictable pattern of organ injury. However, occult injuries can be overlooked, resulting in devastating complications.

Assessment
o Examination of the abdomen in a patient who is awake may indicate peritoneal signs, such as pain and guarding and
rebound tenderness, which necessitate exploration without delay.
o Abdominal distension in an unresponsive patient may indicate active internal bleeding that also requires exploration,
especially in combination with hypotension.
o Rectal examination is performed on all patients with penetrating abdominal trauma, as blood per rectum and high-riding
prostate can indicate bowel injury and genitourinary tract injury, respectively.
o Notation of blood at the urethral meatus is also a sign of genitourinary tract injury.
o Upon arrival at the emergency department, communication of the incident history and the patient’s vital signs to the
emergency or trauma team is of paramount importance. Advanced trauma life support protocols are initiated. Airway protection
and ventilatory support are followed by circulatory resuscitation with fluid infusion. Patients who present with hypotension are
already in class III shock (30-40% blood volume loss), and they should receive blood products as soon as possible.

Diagnostic Findings:
All patients should undergo certain basic laboratory testing, as follows:
• Complete blood count (CBC) provides a baseline value for later comparison, even though it may not reveal the extent of
active bleeding.
• Basic chemistry profile (BMP) also reveals any baseline renal insufficiency or electrolyte abnormalities.
• Coagulation studies (PT/INR + PTT) may suggest development of coagulopathy.
• Arterial blood gas (ABG) provides important information regarding acid-base balance and, thus, the hemodynamic stability
of the patient.
• Urine dipstick may reveal occult blood indicative of genitourinary tract injuries. Female patients should have urine
pregnancy testing.
Imaging Studies
Many imaging modalities can be useful in the evaluation of a patient with penetrating abdominal trauma.
Plain radiograph
Chest radiograph is obtained on all patients because penetration of the chest cavity cannot be ruled out, even with abdominal
stab wounds or even-numbered GSWs.
Ultrasound
Used to evaluate for pericardial fluid indicative of cardiac injury and for free peritoneal fluid. Free fluid in the abdomen can be a
sign of hemorrhage secondary to liver or splenic laceration or, less commonly, of spillage secondary to hollow viscus injury.

CT scan
CT scan is used in the evaluation of patients with stab wounds to the flank and the back and in the evaluation of selected patients
with abdominal stab wounds and GSWs.

Rigid sigmoidoscopy
Patients with blood on rectal examination who are otherwise being managed expectantly (mostly stab wounds) should undergo
rigid sigmoidoscopy to rule out rectal injury.

Diagnostic peritoneal lavage (DPL)

o Can be performed via either a closed method (ie, small skin puncture with blind insertion of catheter over guidewire) or an
open method (ie, insertion of catheter under direct vision after exposure of the peritoneum through a small infraumbilical
incision).
o Aspiration of gross blood is positive for peritoneal penetration and organ injury. The fluid is then evaluated for the
presence of red blood cells (>10,000/mm3), white blood cells (>500/mm3), bile, fibers, or particles, any of which indicate
peritoneal penetration and organ injury.
Management
• GSWs are associated with a high incidence of intra-abdominal injuries. Nearly all patients with GSWs require laparotomy.
• Patients who arrive in shock should be typed and crossed for 4-8 units packed red blood cells.
• Nasogastric intubation
o All patients undergoing endotracheal intubation require decompression of the stomach to decrease the risk of aspiration.
Blood in the nasogastric tube can indicate upper gastrointestinal injury.
• Foley catheterization
o Catheter insertion is required to monitor the fluid resuscitation status of the patient with penetrating abdominal trauma.
The presence of blood in the urine is a sign of genitourinary tract injury.
• Tube thoracostomy
o Patients with penetrating wounds to the thoracoabdominal area may require chest tube placement. Absent or significantly
decreased unilateral breath sounds necessitate immediate tube thoracostomy to relieve hemothorax/pneumothorax. In other
patients, hemothorax/pneumothorax will be identified on chest radiograph.
• Resuscitation of the patient with penetrating abdominal trauma begins immediately upon arrival.
• Fluids should be administered rapidly. Normal saline or Ringer’s lactate solution can be used for crystalloid resuscitation.
Patients arriving in shock or with obvious significant bleeding should receive blood products as quickly as possible. Arterial access
for continuous blood pressure monitoring is standard.
• Efforts should be made to limit hypothermia, including warm blankets and prewarmed fluids. Antibiotics should be
administered to patients undergoing exploration.
Surgical Mangement

Essential components to the trauma laparotomy include:

• control of bleeding,
• identification of injuries,
• control of contamination, and
• reconstruction (if possible).

• Depending on the character of the defect(s), resection may be necessary. If the patient is stable enough to continue the
operation, reconstruction may then be performed.

Postoperative Details
• Occasionally, patients with penetrating abdominal trauma develop such significant metabolic acidosis and coagulopathy
that proceeding with the reconstruction phase of the laparotomy is not possible.
• In these cases, the operation is considered damage-control surgery, and the abdomen is closed rapidly. Often, a
temporary closure with an intravenous fluid bag or mesh (occasionally with a vacuum dressing) is used, as the patient has
undergone massive fluid resuscitation and the bowel has become quite edematous, precluding primary closure of the abdomen.
The patient is then transported to the intensive care unit for continued resuscitation and warming. Reconstruction then takes
place upon return to the operating room in 24-48 hours.
• Attention should be paid to:
o warming the patient,
o continuing fluid and blood product resuscitation,
o replacing electrolytes, and
o monitoring drain outputs

Complications
• Early postoperative complications include ongoing bleeding, coagulopathy, and abdominal compartment syndrome.
• The latter is treated with opening of the abdomen and temporary closure.
• Later complications include acute respiratory distress syndrome, pneumonia, sepsis, intra-abdominal fluid collections,
wound infections, and enterocutaneous fistulae.
• Late complications include small bowel obstruction and incisional hernias.