Diagnostic Tests for Major Trauma
Test	Purpose	Abnormal Findings
*Blood Studies*
Type and screen/type and cross-match	To have type-specific and cross-matched blood available for resuscitation	Inability to cross-match if specimen is collected after multiple units of blood are transfused.
Arterial blood gas (ABG)	Assess for adequacy of oxygenation and ventilation and to determine the level of anaerobic metabolism.	pH <7.35 with increased PaCO₂ (>45 mm Hg) indicates respiratory acidosis. Serum bicarbonate <22 mEq/L with a pH <7.35 can indicate metabolic acidosis. Decreased PaO₂ indicates hypoxemia. Increased PaCO₂ indicates inadequate ventilation. Base deficit <−2.0 mEq/L indicates increased oxygen debt.
Complete blood count (CBC) Hemoglobin (Hgb) Hematocrit (Hct)	Assess for blood loss.	Decreased Hgb and Hct indicate blood loss. Often Hgb and Hct are within normal range initially, especially if the patient has not received a significant amount of fluid to replace the blood loss. The Hgb and Hct should be repeated after the patient has a fluid challenge if there is any indication of significant bleeding.
Electrolytes Potassium (K⁺) Glucose Creatinine	Provide a baseline and assess for possible alterations.	Potassium may be elevated with crush injuries. Glucose is usually elevated after injury. Decreased glucose indicates hypoglycemia and may cause decreased level of consciousness. Elevated creatinine indicates decreased renal functioning, and care should be taken when administering contrast for radiologic studies.
Coagulation profile Prothrombin time (PT) with international normalized ratio (INR) Partial thromboplastin time (PTT) Fibrinogen D-dimer	Assess for causes of bleeding, clotting and disseminated intravascular coagulation (DIC) indicative of abnormal clotting present in shock or ensuing shock.	Decreased PT with low INR promotes clotting; elevation promotes bleeding; elevated fibrinogen and D-dimer reflect abnormal clotting is present.
Blood alcohol	To determine the level of alcohol in the patient’s blood	>10 mg/dl indicates the presence of alcohol in the patient’s blood. The higher the level, the more chance the patient has of showing signs of intoxication, but an absolute value will depend on the patient’s tolerance. This may interfere with neurologic assessment.
Carbohydrate deficient transferring (CDT)	To identify patients who have had excessive drinking for the past few weeks and may be at risk for alcohol withdrawal	>20 units/L for males and >26 units/L for females indicate excessive drinking.
Drug screen	To identify the presence of drugs in the patient”s system	Positive value indicates recent use of the substance.
*Radiology*
Chest radiograph (CXR)	Assess thoracic cage (for fractures), lungs (pneumothorax, hemothorax); size of mediastinum, size of heart.	Displaced lung margins will be present with pneumothoraces and hemothoraces. Cardiac enlargement may reflect cardiac tamponade.
Pelvic radiograph	Assess the integrity of the pelvic ring to indentify fractures and determine stability of the pelvis.	Fracture lines through any of the bones in the pelvis, widening of the symphysis pubis, and widening of the sacroiliac joint(s)
Computerized tomography head, neck, chest, abdomen, and/or pelvis	Assess for internal injuries.	Any findings of skeletal fractures, misalignment, organ damage, or abnormal collections of blood indicates injury to the organ/tissue involved.
Ultrasound: FAST Focused Assessment with Sonography for Trauma	Assess for fluid around the heart, liver, spleen and bladder.	Abnormal collection of fluid
*Invasive Studies*
Diagnostic peritoneal lavage (DPL)	Assess for blood or in the peritoneal cavity or abnormal substrates in the peritoneal lavage fluid.	The presence of red or white blood cells, bile, food fibers, amylase, or feces in the lavage fluid suggests injury to the abdominal organs. Lavage fluid coming from the Foley catheter indicates bladder rupture. Lavage fluid coming from the chest tube, if present, indicates diaphragm rupture.

Collaborative management

The primary goals of initial assessment in major trauma are to identify life-threatening injuries, stop bleeding, and restore adequate oxygenation to the tissues. Once life-threatening injuries have been addressed, a secondary assessment is performed to indentify all injuries the patient may have sustained. It is important to perform a thorough organized head-to-toe assessment to minimize the chance of missing injuries. The following treatments may be required:

Care priorities

1. Secure a patent airway:

A patent airway must be secured when a GCS score less than 8 or potential for airway compromise is possible and/or the patient has respiratory failure requiring mechanical ventilation. The airway is secured by intubation using a rapid sequence intubation protocol to prevent patient movement during the procedure. If the patient is unable to be intubated, a surgical airway must be performed. The surgical airway of choice in an emergency situation is a cricothyroidotomy. If the cervical spine has not been cleared, the spine must be stabilized during the procedure by maintaining constant in-line positioning with gentle traction.

2. Support ventilation:

If the patient is not adequately ventilating to maintain oxygen saturations above 95%, the patient should be placed on supplemental oxygen. Most major trauma patients will require supplemental oxygen. Blood loss creates reduced oxygen-carrying capacity, and tissue demand for oxygen is greatly increased during the hypermetabolic phase. High-flow oxygen by mask is indicated initially. Oxygen therapy can be titrated according to ABG and pulse oximetry values. Mechanical ventilation may be required if the patient is not ventilating well enough to remove CO₂. If the patient does not have equal breath sounds, a pneumothorax or hemothorax should be suspected and a tube thoracotomy may be indicated.

3. Manage hemorrhage and hypovolemia:

Stopping blood loss and restoring adequate circulating blood volume are imperative. Lack of resuscitation will lead to increasing oxygen debt and eventually to MODS and death. The goal of resuscitation in any trauma patient should be to restore adequate tissue perfusion. Two or more large-bore (XXgw:math1XX^ZZgw:math1ZZ16-gauge) short catheters should be placed to maximize delivery of fluids and blood. Use of intravenous (IV) tubing with an exceptionally large internal diameter (trauma tubing), absence of stopcocks, and use of external pressure are techniques used to promote rapid fluid volume therapy when indicated. In some cases the patient may require large central venous access, such as an 8.5 Fr introducer. When rapid infusion of large amounts of fluid is required, all fluid should be warmed to body temperature to prevent hypothermia. Rapid warmer/infuser devices are available to facilitate rapid administration of blood products. Fluid resuscitation should be used more judiciously in pediatric and older patients, as well as patients with significant craniocerebral trauma, who have precise fluid requirements (see Traumatic Brain Injury, p. 341).

• Crystalloids: Initial fluid used for resuscitation should be an isotonic electrolyte solution such as 0.9% normal saline (NS), or lactated Ringer’s (LR). Other balanced electrolyte solutions, such as Normosol-R pH 7.4 (Hospira) or Plasmalyte-A 7.4 (Baxter) may be used after initial fluid resuscitation has been completed.

• Rapid bolus: From 1 to 2 L of rapid IV fluid infusion for adults and 20 ml/kg for pediatric patients should be initiated in the prehospital setting. If the patient continues to show signs of shock after the bolus is complete, blood transfusions should be considered.

• Packed red blood cells (PRBCs): Typed and cross-matched blood is ideal, but in the immediate resuscitation period, if cross-matched blood is not available, type O blood may be used. Once the patient has been typed, type-specific blood can be used. Those patients requiring continuous blood transfusions need reassessment to identify the source of bleeding and definitive treatment to stop ongoing blood loss. A massive transfusion protocol may also need to be initiated.

• Massive transfusion is defined as replacement of one half of the patient’s blood volume at one time or complete replacement of the patient’s blood volume over 24 hours. A massive transfusion protocol ensures the patient receives plasma, platelets, and cryoprecipitate in addition to the packed red blood cells to prevent the complications related to coagulopathy. Another concern with massive transfusion is hypocalcemia caused by calcium binding with citrate in stored PRBCs, resulting in depressed myocardial contractility, particularly in hypothermic patients or in those with impaired liver function. One ampule of 10% calcium chloride should be considered for administration after every 4 units of PRBCs.

Only O-negative packed cells should be transfused into prepubescent females and women in childbearing status to prevent sensitization and future complications during pregnancy.

• Autotransfusion: Shed blood from the patient can be collected, filtered, and reinfused. Shed blood is captured from chest tube drainage or the operative field and reinfused immediately. Various techniques are used to capture and reinfuse the blood. Advantages of autotransfusion include reduced risk of disease transmission, absence of incompatibility problems, and availability. Disadvantages include risk of blood contamination and presence of naturally occurring factors that promote anticoagulation.

• Colloids: Resuscitation with colloids has not been shown to reduce mortality and is not used in the initial resuscitation of trauma patients.

• Recombinant factor VIIa (rFVIIa): The standard use of rFVIIa in the resuscitation of trauma patients is still controversial. Some studies have shown a decrease in the number of units of PRBCs required for patients in hemorrhagic shock but have not shown a decrease in mortality. More studies are needed to determine the appropriate indications, contraindications, dosage, and timing of rFVIIa administration in trauma patients experiencing hemorrhagic shock.

4. Identify, prevent, and/or manage hypothermia:

Warmed blankets, forced warm air blankets, and warmers for IV fluids and blood should be used to prevent hypothermia. If the patient is already hypothermic, more aggressive measures to rewarm the patient may be necessary. Warming lights are useful for pediatric patients. Core rewarming measures can include irrigation of the peritoneal and/or thoracic cavities with warmed saline, use of heated humidified oxygen, and extracorporeal blood rewarming.

5. Provide gastric decompression:

Gastric intubation permits gastric decompression, aids in removal of gastric contents, and helps to prevent vomiting or possible aspiration. The nasal route is contraindicated in patients with basilar skull fractures (BSFs) because of the need to prevent tubes entering the cranial vault via abnormal openings in the fractured skull. In patients with facial trauma or suspected or known BSF, gastric tubes should be placed orally.

6. Ensure urinary drainage:

An indwelling catheter is inserted to obtain a specimen for urinalysis and to monitor hourly urine output. See Renal and Lower Urinary Tract Trauma, p. 317, for precautions.

7. Prevent infection with antibiotics:

Broad-spectrum antibiotics are used initially to prevent infections if there are open wounds or compound fractures. More specific antimicrobial agents are used when results from culture and sensitivity tests are available.

8. Control pain and anxiety with analgesics and anxiolytics:

Relief of pain and anxiety are accomplished using IV opiates and anxiolytics. All IV agents should be carefully titrated to desired effect, while avoiding respiratory depression, masking injury, or disguising changes in physiologic parameters. Use of the World Health Organization (WHO) ladder for pain management and a pain-rating scale are essential for the trauma population.

9. Provide tetanus prophylaxis:

Tetanus immunoglobulin and tetanus-toxoid are considered on the basis of Centers for Disease Control and Prevention (CDC) recommendations (Table 3-1).

Table 3-1 GUIDE TO TETANUS PROPHYLAXIS IN ROUTINE WOUND MANAGEMENT

10. Initiate nutritional support therapy:

Infection and sepsis contribute to the negative nitrogen state and increased metabolic needs. Prompt initiation of nutrition therapy is essential for rapid healing and prevention of complications. Parenteral nutrition or postpyloric (jejunal) feedings may be used if postoperative ileus or injury to the gastrointestinal (GI) tract is present. For more information, see Nutritional Support, p. 117.

11. Facilitate evaluation for surgery:

Need for surgery depends on the type and extent of injuries. The surgical team is coordinated by the trauma surgeon. When several specialty surgeons are required for various injuries, the order of surgeries is coordinated carefully to preserve life and limit the potential for disability.

CARE PLANS: MAJOR TRAUMA

Ineffective tissue perfusion, cardiopulmonary

Goals/outcomes

Within 24 hours of this diagnosis, patient exhibits adequate tissue perfusion, as evidenced by BP within normal limits for patient, heart rate (HR) 60 to 100 beats per minute (bpm), normal sinus rhythm on electrocardiogram (ECG), peripheral pulses greater than 2+ on a 0-to-4+ scale, warm and dry skin, hourly urine output ≥0.5 ml/kg, base deficit between +2 and −2 mmol/L, serum lactate less than 2.2 mmol/L, measured cardiac output (CO) 4 to 7 L/min, pulmonary artery wedge pressure (PAWP) 6 to 12 mm Hg, and patient awake, alert, and oriented.

Blood Loss Severity

Shock management: volume

1. Monitor for sudden blood loss or persistent bleeding.

2. Prevent blood volume loss (e.g., apply pressure to site of bleeding).

3. Monitor for fall in systolic BP to less than 90 mm Hg or a fall of 30 mm Hg in hypertensive patients.

4. Monitor for signs/symptoms of hypovolemic shock (e.g., increased thirst, increased HR, increased systemic vascular resistance (SVR), decreased urinary output [urine output], decreased bowel sounds, decreased peripheral perfusion, altered mental status, or altered respirations).

5. Position the patient for optimal perfusion.

6. Insert and maintain large-bore IV access.

7. Administer warmed IV fluids, such as isotonic crystalloids, as indicated.

8. Administer blood products (e.g., PRBCs, platelets, plasma, and cryoprecipitate) as appropriate.

9. Administer oxygen and/or mechanical ventilation, as appropriate.

10. Draw arterial blood gases and monitor tissue oxygenation.

11. Monitor Hgb/hematocrit (Hct) level.

12. Monitor coagulation studies, including INR, PT, PTT, fibrinogen, fibrin degradation/split products, and platelets.

13. Monitor lab studies (e.g., serum lactate, acid-base balance, metabolic profiles, and electrolytes).

14. Monitor fluid status, including intake and output, as appropriate.

15. Monitor for clinical signs and symptoms of overhydration/fluid excess.

Vital signs monitoring

1. Monitor BP, pulse, temperature, and respiratory status, as appropriate.

2. Note trends and wide fluctuations in BP.

3. Auscultate BPs in both arms and compare, as appropriate.

4. Initiate and maintain a continuous temperature monitoring device, as appropriate.

5. Monitor for and report signs and symptoms of hypothermia and hyperthermia.

6. Monitor the presence and quality of pulses.

7. Monitor cardiac rate and rhythm.

Acid-base monitoring

1. Examine the pH level in conjunction with the PaCO₂ and HCO₃ levels to determine whether the acidosis/alkalosis is compensated or uncompensated.

2. Monitor for an increase in the anion gap (greater than 14 mEq/L), signaling an increased production or decreased excretion of acid products.

3. Monitor base excess/base deficit levels.

4. Monitor arterial lactate levels.

5. Monitor for elevated chloride levels with large volumes of NS.

Impaired gas exchange

Goals/outcomes

Within 12 to 24 hours of treatment, patient has adequate gas exchange as evidenced by PaO₂ ≥80 mm Hg, PaCO₂ 35 to 45 mm Hg, pH 7.35 to 7.45, presence of normal breath sounds, and absence of adventitious breath sounds. RR is 12 to 20 breaths/min with normal pattern and depth (eupnea).

Respiratory Status: Gas Exchange; Respiratory Status: Ventilation

Airway management

1. Assess for patent airway; if snoring, crowing, or strained respirations are present, indicative of partial or full airway obstruction, open airway using chin-lift or jaw-thrust and maintain cervical spine alignment.

2. Insert oral or nasopharyngeal airway if patient cannot maintain patent airway; if severely distressed, patient may require endotracheal intubation.

3. When spine is cleared, position patient to alleviate dyspnea and ensure maximal ventilation, generally in a sitting inclined position unless severe hypotension is present.

4. Clear secretions from airway by having patient cough vigorously, or provide nasotracheal, oropharyngeal, or endotracheal tube suctioning as needed.

5. Have patient breathe slowly or manually ventilate with bag-valve-mask device slowly and deeply between coughing or suctioning attempts.

6. Assist with use of incentive spirometer as appropriate.

7. Turn patient every 2 hours if immobile. Encourage patient to turn self, or get out of bed as much as tolerated if patient is able.

8. Provide chest physical therapy as appropriate, if other methods of secretion removal are ineffective.

Oxygen therapy

1. Provide humidity in oxygen.

2. Administer supplemental oxygen using liter flow and device as ordered.

3. Restrict patient and visitors from smoking while oxygen is in use.

4. Document pulse oximetry with oxygen liter flow in place at time of reading as ordered. Oxygen is a drug; the dose of the drug must be associated with the oxygen saturation reading or the reading is meaningless.

5. Obtain arterial blood gases if patient experiences behavioral changes or respiratory distress to check for hypoxemia or hypercapnia.

6. Monitor for changes in chest radiograph and breath sounds indicative of oxygen toxicity and absorption atelectasis in patients receiving higher concentrations of oxygen (FIO₂ greater than 45%) for longer than 24 hours. The higher the oxygen concentration, the greater is the chance of toxicity.

7. Monitor for skin breakdown where oxygen devices are in contact with skin, such as nares and around edges of mask devices.

8. Provide oxygen therapy during transportation and when patient gets out of bed.

Respiratory monitoring

1. Monitor rate, rhythm, and depth of respirations.

2. Note chest movement for symmetry of chest expansion and signs of increased work of breathing such as use of accessory muscles or retraction of intercostal or supraclavicular muscles.

3. Ensure airway is not obstructed by tongue (snoring or choking-type respirations) and monitor breathing patterns. New patterns that impair ventilation should be managed as appropriate for setting.

4. Note that trachea remains midline, as deviation may indicate patient has a tension pneumothorax.

5. Auscultate breath sounds following administration of respiratory medications to assess for improvement.

6. Note changes in oxygen saturation (SaO₂), pulse oximetry (SpO₂), end-tidal CO₂ (ETCO₂), and ABGs as appropriate.

7. Monitor for dyspnea and note causative activities/events.

8. If increased restlessness or unusual somnolence occurs, evaluate patient for hypoxemia and hypercapnia as appropriate.

9. Monitor chest x-ray reports as new films become available.

Acute pain

related to physical injury

Goals/outcomes

Within 30 minutes of intervention, patient’s subjective evaluation of discomfort improves, as documented by a pain scale. Nonverbal indicators, such as grimacing, are absent. Vital signs return to baseline. ECG changes present during event resolve.

Comfort Status: Physical, Pain Level

Pain management

1. Assess and document the location and intensity of the pain. Devise a pain scale with patient, rating discomfort from 0 (no pain) to 10 or any system that assists in objectively reporting pain level. If intubated, use a physiologic scale such as adult nonverbal pain scale or the FLACC scale.

2. Determine the needed frequency of making an assessment of patient comfort and implement monitoring plan.

3. Provide the patient with optimal pain relief with prescribed analgesics.

4. Ensure pretreatment analgesia and/or nonpharmacologic strategies prior to painful procedures.

5. Evaluate the effectiveness of the pain control measures used through ongoing assessment of the pain experience.

Hypothermia

Goals/outcomes

Patient will maintain a normal body temperature above 36°C (96.8°F).

Thermoregulation

Temperature regulation

1. Monitor temperature at least every 2 hours, as appropriate.

2. Institute a continuous core temperature monitoring device, as appropriate.

3. Monitor BP, pulse, and respirations, as appropriate.

4. Monitor skin color and temperature.

Posttrauma syndrome

Goals/outcomes

Patient exhibits appropriate coping mechanism and reduced anxiety as evidenced by decreased restlessness, pulse rate 60 to 100 bpm, respiratory rate 12 to 20 breaths/min, and decrease in the amount of pain medication requested.

Anxiety Level; Coping

Coping enhancement

1. Provide an atmosphere of acceptance.

2. Provide the patient with realistic choices about certain aspects of care.

3. Acknowledge the patient’s spiritual/cultural background.

4. Encourage the use of spiritual resources, if desired.

5. Encourage verbalization of feelings, perceptions, and fears.

6. Assist the patient to identify available social supports.

7. Encourage family involvement, as appropriate.

Emotional support

1. Make supportive and empathetic statements.

2. Encourage the patient to express feelings of anxiety, anger, or sadness.

3. Refer for counseling, as appropriate.

Additional nursing diagnoses

Also see nursing diagnoses and interventions as appropriate in Nutritional Support (p. 117), Mechanical Ventilation (p. 99), Hemodynamic Monitoring (p. 75), Prolonged Immobility (p. 149), and Emotional and Spiritual Support of the Patient and Significant Others (p. 200).

Abdominal trauma

Pathophysiology

The patient with abdominal injury can be the most challenging and difficult to manage. Forces may be blunt or penetrating and the organs are either solid (pancreas, kidneys, adrenal glands, liver, and spleen) or hollow (stomach, small bowel, and colon).This patient may have subtle signs of internal hemorrhage, which can be a major contributor to the increase in mortality and morbidity noted after the initial injury has been managed. The severity of abdominal injury is related to the type of force applied to the organs suspended inside the peritoneum. Motor vehicle collision (MVC), either auto-auto or auto-pedestrian, is the most common cause of blunt abdominal trauma worldwide.

Blunt trauma

There are three mechanisms of action with blunt trauma.

1. Rapid deceleration: On impact, the different organs that reside inside abdominal cavity move at different speeds depending on their density. This creates what is known as shear force, that is, two different directions applied to the organ, usually at the point of attachment, causing injury to other organs such as the aorta.

2. Crush of contents between the walls: Solid viscera are exceptionally affected when the compression occurs from the anterior abdominal wall and the spine or posterior cage.

3. External compression force: The force of external traumatic impact may increase the organ and abdominal pressures to such a degree that the hollow organs rupture.

Mechanisms of action with penetrating injury

External penetration to the abdominal cavity can be caused by any missile or object that intrudes into the abdominal cavity. Penetrating forces injure the organ(s) in the direct path of the instrument or missile, while shock waves from high-velocity weapons (e.g., high-powered rifles) may also injure adjacent organs. Stab wounds are generally easier to manage than gunshot wounds but may be fatal if a major blood vessel (aorta) or highly vascular organ (liver) is penetrated. The three most common injuries associated with penetrating abdominal trauma are those to the small bowel, liver, and colon. With blunt trauma, injuries to the liver, spleen, and kidney are more common. Undetected mesenteric damage may cause compromised blood flow, with eventual bowel infarction. Perforations or contusions result in release of bacteria and intestinal contents into the abdominal cavity, causing serious infection.

The abdomen can be divided into four areas: (1) intrathoracic abdomen, (2) pelvic abdomen, (3) retroperitoneal abdomen, and (4) true abdomen.

Intrathoracic abdomen:

The upper abdomen resides beneath the rib cage and includes the diaphragm, liver, spleen, and stomach.

• Diaphragm: Commonly injured at the left posterior portion after blunt trauma, the tear is best visualized by chest radiograph, which reveals an elevation of the left hemidiaphragm and air under the diaphragm.

• Spleen: The organ most frequently injured after blunt trauma, massive hemorrhage from splenic injury is common. Damage to the spleen may occur with the most trivial of injuries, so index of suspicion should be high. Splenic injury is often associated with hepatic or pancreatic injury due to close proximity of these organs. Splenectomy is the treatment of choice for major spleen injuries. Minor splenic injuries may be managed with direct suture techniques

• Liver: Most frequently involved in penetrating trauma (80%) because of its large size and location, the liver is less often affected by blunt injury (20%). Control of bleeding and bile drainage is the priority with hepatic injury. Mortality from liver injuries is about 10%. In most patients, bleeding from a liver injury can be controlled, such as with perihepatic packing. About 5% of injuries require packing for bleeds. Major arterial bleeding from the liver parenchyma will require further attention. Biliary tree injuries may require surgical repair and should be suspected with liver injury. The patient may be asymptomatic or have mild to moderate abdominal discomfort with biliary tree injury.

Pelvic abdomen:

As defined by bony pelvis, this includes the urinary bladder, urethra, rectum, small intestine, and, in females, the ovaries, fallopian tubes, and uterus. Diagnosis is difficult becauses many of these injuries are extraperitoneal (outside the peritoneal cavity).

Retroperitoneal abdomen:

This includes the kidneys, ureters pancreas, aorta, and vena cava. Evaluation may require a computed tomography (CT) scan, angiography, and an IV pyelogram.

• Retroperitoneal vessels: Tears in retroperitoneal vessels associated with pelvic fractures or damage to retroperitoneal organs (pancreas, duodenum, and kidney) can cause bleeding into the retroperitoneum.

• Although the retroperitoneal space can accommodate up to 4 L of blood, detection of retroperitoneal hematomas is difficult and sophisticated diagnostic techniques may be required.

True abdomen:

This includes the small and large intestines, uterus (when enlarged), and bladder (when distended). Perforation usually presents with peritonitis such as pain and tenderness.

• Colon: Injury is most frequently caused by penetrating forces, although lap belts, direct blows, and other blunt forces cause a small percentage of colonic injuries. Because of the high bacterial content, infection is even more a concern than it is with small bowel injury. Most patients with significant colon injuries require a temporary colostomy.

• Undetected mesenteric damage: May cause compromised blood flow, with eventual bowel infarction. Perforations or contusions result in release of bacteria and intestinal contents into the abdominal cavity, causing serious infection.

• Pelvis: See Renal and Lower Urinary Tract Trauma, p. 317.

Occasionally the lower portion of the esophagus is involved in penetrating trauma. The stomach is usually not injured with blunt trauma since it is flexible and readily displaced, but it may be injured by direct penetration. Injury to either the esophagus or stomach results in the escape of irritating gastric fluids due to gastric perforation and the release of free air below the level of the diaphragm. Esophageal injuries often are associated with thoracic injuries. Once hemorrhage has been controlled, attention is turned to prevention of further contamination by controlling spillage of gut contents.

Traumatic pancreatic or duodenal injury is uncommon but is associated with high morbidity and mortality. These injuries are difficult to detect and may be associated with massive injury to nearby organs, prompting spillage of irritating fluids, activated enzymes, and bile, which augments the inflammatory response. Pancreatic injury is rare; however, the pancreas can be contused or lacerated. Clinical indicators of injury to these retroperitoneal organs may not be obvious for several hours.

Injuries to major vessels such the abdominal aorta and inferior vena cava most often are caused by penetrating trauma but also occur with deceleration injury. Hepatic vein injuries frequently are associated with juxtahepatic vena caval injury and result in rapid hemorrhage. Blood loss after major vascular injury is massive. Survival depends on rapid transport to a trauma center and immediate surgical intervention.

Assessment: abdominal trauma

Goal of system assessment

Rapidly evaluate for significant primary and secondary injuries (for all systems) while performing basic and advanced trauma life support. Airway, breathing, circulation, disability, and exposure are the structural components of all trauma assessment.

In an unstable patient, immediate identification of free intra-abdominal fluid by Focused Assessment with Sonography for Trauma (FAST) examination or a diagnostic peritoneal lavage (DPL) is imperative and supports decisions to move straight to the operating room.

In the traditional perspective of the “Golden Hour of Trauma” (period of time immediately after traumatic injury in which rapid intervention may prevent death), the American College of Surgeons (ACS) guideline recommends that rapid assessment of hemorrhage includes aggressive volume resuscitation.

History and risk factors

First and foremost, it is essential to establish issues involved with the injury event (Box 3-1). These details regarding circumstances of the accident and mechanism of injury are invaluable in detecting the presence of specific injuries. Second, allergies, medications, and last meal eaten will play an important role in the maintenance of good resuscitation. Other information, previous abdominal surgeries, and use of safety restraints (if appropriate) should be noted. Hollow viscous injury is often missed but should always be suspected with a visible contusion on the abdomen. Medical information including current medications and last tetanus-toxoid immunization should be obtained. The history is sometimes difficult to obtain because of alcohol or drug intoxication, head injury, breathing difficulties, or impaired cerebral perfusion. Family members and emergency personnel may be valuable sources of information.

Vital signs

Assess for impending hemorrhagic shock: Pulse greater than 100 bpm, decreased pulse pressure, oliguria: blood loss 750 to 1500 ml; pulse greater than 120, hypotension, oliguria, confusion: blood loss 1500 to 2000 ml; pulse greater than 140, severe oliguria, lethargy: blood loss greater than 2000 ml .

HIGH ALERT!

Persistent Tachycardia

Persistent tachycardia should always be considered a clue to tissue hypoxia. As the neuroendocrine response ensues, persistent tachycardia should warn all observers that there is response to tissue signals of hypermetabolism and inadequate resuscitation.

• Hypotension: Presence of hypotension is a sign of impending doom, but the absence of hypotension does not always accurately reflect an absence of hemorrhage. After an injury, a profound neuroendocrine response ensues to activate the beta receptors (sinus node and ventricular contractile tissue), the alpha receptors (smooth muscle in the arteries), and the renal tubules (promoting preservation of fluid), resulting in significant tachycardia, profound vasoconstriction, and progressive oliguria. These responses may mask the severity of hemorrhage. Patients on alpha or beta antagonists or those with acute spinal cord injuries (above C5) will not manifest these responses and therefore will have few compensatory mechanisms.

• Pulse pressure: This measure may be effectively used to determine the amount of volume in the arteries (systolic minus diastolic BP, normal greater than 40 mm Hg). Pulse pressure generally correlates with the volume ejected by the left ventricle and therefore is a valuable tool for indication of volume in the vascular bed. Presence of pulsus paradoxus (Box 3-2) may be visualized with either the invasive arterial pressure trace or the plethysmograph of the pulse oximeter and is an invaluable tool in evaluating arterial volume.

Box 3-2 MEASURING PARADOXICAL PULSE

• After placing BP cuff on patient, inflate it above the known systolic BP. Instruct patient to breathe normally.

• While slowly deflating the cuff, auscultate BP.

• Listen for the first Korotkoff sound, which will occur during expiration with cardiac tamponade.

• Note the manometer reading when the first sound occurs, and continue to deflate the cuff slowly until Korotkoff sounds are audible throughout inspiration and expiration.

• Record the difference in millimeters of mercury between the first and second sounds. This is the pulsus paradoxus.

Observation and subjective/objective symptoms

• Inspection of all surfaces of trunk, head, neck, and extremities, including anterior lateral and posterior exposure, with notation of all penetrating wounds, contusions, tenderness, ecchymosis, or other marks and indicators. Multiple wounds may represent entrance or exit wounds but do not eliminate the possibility of objects that may remain internally.

• Kehr sign (left shoulder pain caused by splenic bleeding) also may be noted, especially when the patient is recumbent.

• Nausea and vomiting may occur, and the conscious patient who has sustained blood loss often complains of thirst—an early sign of hemorrhagic shock.

• Preoperative pain is anticipated and is a vital diagnostic aid. The nature of postoperative pain also can be important. Incisional and some visceral pain can be anticipated, but intense or prolonged pain, especially when accompanied by other peritoneal signs, can signal bleeding, bowel infarction, infection, or other complications.

It is important to note that damage to retroperitoneal organs such as the pancreas and duodenum may not cause significant signs and symptoms for 6 to 12 hours or longer. Relatively slow bleeding from abdominal viscera may not be clinically apparent for 12 hours or longer after the initial injury. In addition, the nurse should be aware that complications such as bowel obstruction caused by adhesions or narrowing of the bowel wall from localized ischemia, inflammation, or hematoma may develop days or weeks after the traumatic event. The need for vigilant observation in the care of these patients cannot be overemphasized.

Inspection

• Abrasions and ecchymoses may indicate underlying injury. The absence of ecchymosis does not exclude major abdominal trauma and massive internal bleeding. In the event of gunshot wounds, entrance and exit (if present) wounds should be identified.

• Ecchymosis over the left upper quadrant (LUQ) suggests splenic rupture, and erythema and ecchymosis across the lower portion of the abdomen suggest intestinal injury caused by lap belts.

• Grey-Turner sign, a bluish discoloration of the flank, may indicate retroperitoneal bleeding from the pancreas, duodenum, vena cava, aorta, or kidneys.

• Cullen sign, a bluish discoloration around the umbilicus, may be present with intraperitoneal bleeding from the liver or spleen. Ecchymosis may take hours to days to develop, depending on the rate of blood loss.

Auscultation

It is important to auscultate before palpation and percussion, because these maneuvers can stimulate the bowel and confound assessment findings.

• Bowel sounds: These are likely to be decreased or absent with abdominal organ injury or intraperitoneal bleeding. The presence of bowel sounds, however, does not exclude significant abdominal injury. Immediately after injury, bowel sounds may be present, even with major organ injury. Bowel sounds should be auscultated in each quadrant every 1 to 2 hours in patients with suspected abdominal injury. Absence of bowel sounds is expected immediately after surgery. Failure to auscultate bowel sounds within 24 to 48 hours after surgery suggests ileus, possibly caused by continued bleeding, peritonitis, or bowel infarction.

Palpation

• Tenderness to light palpation suggests pain from superficial or abdominal wall lesions, such as that occurring with seatbelt contusions.

• Deep palpation may reveal a mass, which may indicate a hematoma. Internal injury with bleeding or release of GI contents into the peritoneum results in peritoneal irritation and certain assessment findings. Box 3-3 describes signs and symptoms that suggest peritoneal irritation.

• Subcutaneous emphysema of the abdominal wall is usually caused by thoracic injury but also may be produced by bowel rupture.

• Measurements of abdominal girth may be helpful in identifying increases in girth attributable to gas, blood, or fluid. Visual evaluation of abdominal distention is a late and unreliable sign of bleeding.

• Peritoneal signs (pain, guarding, rebound tenderness) or abdominal distention in an unconscious patient requires immediate evaluation in either case.

Box 3-3 SIGNS AND SYMPTOMS THAT SUGGEST PERITONEAL IRRITATION

• Generalized abdominal pain and tenderness

• Involuntary guarding of the abdomen

• Abdominal wall rigidity

• Rebound tenderness

• Abdominal pain with movement or coughing

• Decreased or absent bowel sounds

HIGH ALERT!

Flank (Grey-Turner sign) or umbilical (Cullen sign) ecchymosis may be delayed several hours to days in patients with retroperitoneal hemorrhage. Based on index of suspicion, persistent hypotension is always investigated with ultrasound or radiography.

• Mild tenderness to severe abdominal pain may be present, with the pain either localized to the site of injury or diffuse.

• Blood or fluid collection within the peritoneum causes irritation that results in involuntary guarding, rigidity, and rebound tenderness.

• Fluid or air under the diaphragm may cause referred shoulder pain.

Percussion

• Unusually large areas of dullness may be percussed over ruptured blood-filled organs. For example, a fixed area of dullness in the LUQ suggests a ruptured spleen. An absence (or decrease in the size) of liver dullness may be caused by free air below the diaphragm, a consequence of hollow viscous perforation, or, in unusual cases, displacement of the liver through a ruptured diaphragm.

• The presence of tympany suggests gas; dullness suggests that the enlargement is caused by blood or fluid.

HIGH ALERT!

Massive intestinal edema is common following laparotomy and prolonged shock. Inflammatory response, neuroendocrine stimulation, aggressive crystalloid resuscitation, bowel handling, intra-abdominal packing, and retroperitoneal hematomas may cause a delay in abdominal closure. If the abdomen is closed, the intra-abdominal volume may compress arteries, capillaries, the bladder, and the ureters. This compartment hypertension (abdominal compartment syndrome) may cause a significant hypotension, oliguria, and base deficit that will be difficult to combat. (See Abdominal Hypertension and Abdominal Compartment Syndrome, p. 861).

Diagnostic Evaluation of Abdominal Trauma
Test	Purpose	Abnormal Findings
FAST: focused assessment with sonography for trauma	Rapid, portable, noninvasive method to detect hemoperitoneum Uses four views to evaluate	Based on the assumption that all clinically significant abdominal injuries are associated with hemoperitoneum. If positive for blood, may require CT. If negative, but suspicious, proceed to DPL.
CT scan	Used to evaluate integrity of cavities and organs	Wound tract outlined by hemorrhage, air, bullet or bone fragments that clearly extend into the peritoneal cavity; the presence of intraperitoneal free air, free fluid, or bullet fragments; and obvious intraperitoneal organ injury
Rectal examination	Evaluate for bony penetration	Blood in the stool (gross or occult) and/or the presence of a high riding prostate (indicates genitourinary or bowel injury)
Chest radiograph (CXR)	Assess size and integrity of heart, thoracic cage and lungs; rules out chest cavity penetration	Hemothoraces or pneumothoraces; air under diaphragm indicates peritoneal penetration.
*Blood Studies*
Complete blood count (CBC) Hemoglobin (Hgb) Hematocrit (Hct) RBC count (RBCs) WBC count (WBCs)	Assess for occult bleeding or effects of gross bleeding	Decreased Hgb or Hct reflects blood loss, may be false negative when patient has lost significant volume. Repeat after 2 L of isotonic fluid resuscitation.
Electrolytes Potassium (K⁺) Magnesium (Mg²⁺) Calcium (Ca²⁺) Sodium (Na⁺)	Assess for possible causes of dysrhythmias and/or heart failure	Decrease in K⁺, Mg²⁺, or Ca²⁺ may cause dysrhythmias. Elevation of Na⁺ may indicate dehydration.
Coagulation profile Prothrombin time (PT) with international normalized ratio (INR) Partial thromboplastin time (PTT) Fibrinogen D-dimer	Assess for causes of bleeding, clotting, and disseminated intravascular coagulation (DIC) indicative of abnormal clotting present in shock or ensuing shock	Decreased PT with low INR promotes clotting; elevation promotes bleeding; elevated fibrinogen and D-dimer reflects abnormal clotting is present.

Collaborative management

The initial focus should be stabilization and supporting hemodynamics, but the highest priority is to diagnose and repair causes of hemorrhage. Timely provision of needed surgery, preferably in a trauma center, is the critical factor impacting survival. Prolonged hypovolemia and shock result in organ ischemia and ultimately failure (see Major Trauma [p. 235], Acute Respiratory Distress Syndrome [p. 365], Cardiogenic Shock [p. 472], Acute Renal Failure [p. 584], Hepatic Failure [p. 785]).

Care priorities

1. Identify and manage hypothermia:

Trauma patients are often profoundly hypothermic on arrival in the emergency department as a result of inadequate protection, IV fluid administration, ongoing blood loss, and environmental exposure. Hemorrhagic shock leads to decreased cellular perfusion and oxygenation and impoverished heat production. Hypothermia interferes with coagulation and platelet aggregation, and therefore exacerbates hemorrhage.

Remove all wet clothing and make sure the patient is dry. The patient should be actively warmed with blankets, air-warming devices, or possibly continuous arteriovenous warming techniques. A simple method is to cover all extremities and the abdomen with plastic (e.g., blue side of underpads or trash bags) to trap all heat produced.

2. Provide oxygen therapy to manage hypoxia:

Abdominal injury may result in poor ventilatory efforts caused by pain or compression of thoracic structures. High-flow supplemental oxygen is indicated initially and then titrated according to ABG values. Mechanical ventilation may be necessary.

3. Manage hypovolemia and anemia:

Because massive blood loss is associated with most abdominal injuries, immediate volume resuscitation is critical. Initially, LR or a similar balanced salt solution is given. Colloid solutions may be helpful in the postoperative period if there are low filling pressures and evidence of decreased plasma oncotic pressure. Typed and cross-matched fresh blood is the optimal fluid for replacement of large blood losses. However, since fresh whole blood is rarely available, a combination of packed cells and fresh frozen plasma often is used. Overaggressive use of colloids and PRBCs may increase third spacing and SIRS. (See Major Trauma, p. 235, for more information.)

• Indication for immediate blood transfusion: Ongoing blood loss indicates hemodynamic instability despite the administration of 2 L of fluid to adult patients.

• Acidosis: Hemorrhagic shock reduces perfusion, resulting in hypoxemia, anaerobic metabolism, and lactic acidosis. The compensatory vasoconstrictive response shunts blood to the heart, lungs, and brain from the skin, muscles, and abdominal organs. Base deficit or lactate levels should be used to guide fluid resuscitation, ventilation, and BP support.

• Coagulopathy: Hypothermia, acidosis, and massive blood transfusion all lead to coagulopathy. The top priority is to stop the bleeding. Coagulopathy is treated by the administration of fresh frozen plasma, factor VII, cryoprecipitate, and platelets and correcting the hypothermia and acidosis. If bleeding persists, consider vasopressin infusion, which causes vasoconstriction and calcium chloride.

4. Consider surgery for penetrating abdominal injuries:

• Indication for emergency laparotomy:

• Signs of peritonitis

• Uncontrolled shock or hemorrhage

• Clinical deterioration during observation

• Positive hemoperitoneum findings with FAST or DPL examinations

• Removing penetrating objects can result in additional injury; thus attempts at removal should be made only under controlled situations with a surgeon and operating room immediately available.

• If evisceration occurs initially or develops later, do not reinsert tissue or organs. Place a saline-soaked gauze over the evisceration, and cover with a sterile towel until the evisceration can be evaluated by the surgeon.

• The issue of mandatory surgical exploration versus observation and selective surgery, especially with stab wounds, remains controversial. There is a trend toward observation of patients without obvious injury or peritoneal signs.

• Indications for laparotomy include one or more of the following: (1) penetrating injury suspected of invading the peritoneum (e.g., abdominal gunshot wound or abdominal stab wound with evisceration, hypotension, or peritonitis); (2) positive peritoneal signs (e.g., tenderness, rebound tenderness, involuntary guarding); (3) shock; (4) GI hemorrhage; (5) free air in the peritoneal cavity as seen on x-ray film; (6) evisceration; (7) massive hematuria; and (8) positive findings on DPL.

The patient should be evaluated for peritoneal signs at least hourly by the same examiner. Consult surgeon immediately if the patient shows peritoneal signs, evidence of shock, gastric or rectal bleeding, or gross hematuria.

5. Consider an appropriate surgical intervention based on type of injury:

• Blunt, nonpenetrating abdominal injuries: Physical examination is important in determining the necessity for surgery in alert, cooperative, nonintoxicated patients. Additional diagnostic tests such as abdominal ultrasound, DPL, or CT are necessary to evaluate the need for surgery in the patient who is intoxicated or unconscious or who has sustained head or spinal cord trauma.

• Immediate laparotomy for blunt abdominal trauma is indicated under the following circumstances: (1) clear signs of peritoneal irritation (see Box 3-3); (2) free air in the peritoneum; (3) hypotension caused by suspected abdominal injury, or persistent and unexplained hypotension; (4) positive DPL findings; (5) GI aspirate or rectal smear positive for blood; and (6) other positive findings in diagnostic tests such as CT or arteriogram.

• Carefully evaluated, stable patients with blunt abdominal trauma may be admitted to a critical care unit for observation. These patients should be evaluated in the same manner as that described in the section Surgical Considerations for Penetrating Abdominal Injuries.

• Need for immediate surgery vs. triad of failure: Once in the operating room, it may become apparent that the patient cannot survive a long procedure, or that the triad of failure (acidosis, hypothermia, and coagulopathy) may cause death. At this point the surgeon may do limited repair and packing, choosing to delay major surgical repair.

• Transfer patient to the ICU, where the triad may be corrected. Survival from abdominal trauma and surgery requires an integrated team effort.

• Focus is to limit the effects of hemorrhage, acidosis, and coagulopathy and to promote perfusion of all organs.

6. Considerations regarding closure of the abdominal surgical incision:

During closure after surgery, if the bowel (intestines) can be visualized with an abdominal horizontal view, the abdomen fascia should not be closed. If the abdomen has been closed, it may become necessary to open it again either in the ICU or the operating room. There are multiple methods discussed in the literature to supplement closure.

1. Silo bag closure: A 3-L sterile plastic irrigation bag is emptied and cut to lie flat. The edges are trimmed and sutured to the skin.

2. Vacuum pack: A 3-L sterile plastic irrigation bag is emptied and cut to lie flat, then placed into the abdomen, and the edges are placed under the sheath. Two suction drains are placed on top of the bag, and a large adherent steridrape is then placed over the whole abdomen. The catheters are placed to suction, providing continuous drainage.

3. Vacuum-assisted closure: This consists of a sterile sponge dressing with an adherent dressing and a continuous negative pressure; it promotes closure, blood flow, and collagen formation.

HIGH ALERT!

Sudden release of the abdominal pressure may lead to further injuries such as ischemia-reperfusion, acute vasodilatation, and cardiac dysfunction and arrest. The nurse should hydrate the patient with at least 2 L of volume. IV fluids and vasopressors should be immediately available in case severe hypotension occurs.

7. Provide nutritional support:

Patients with abdominal trauma have complex nutritional needs because of the hypermetabolic state associated with major trauma and traumatic or surgical disruption of normal GI function. Often infection and sepsis contribute to a negative nitrogen state and increased metabolic needs. Prompt initiation of parenteral or postpyloric feedings, as appropriate, in patients unable to accept conventional enteric feedings and the administration of supplemental calories, proteins, vitamins, and minerals are essential for healing. For additional information, see Nutritional Support, p. 117.

8. Prevention infection with antibiotics:

Abdominal trauma is associated with a high incidence of intra-abdominal abscess, sepsis, and wound infection, particularly with injury to the terminal ileum and colon. Persons with penetrating or blunt trauma and suspected intestinal injury are started on parenteral antibiotic therapy immediately. Broad-spectrum antibiotics are continued postoperatively and stopped after approximately 72 hours unless there is evidence of infection.

9. Manage pain using analgesics:

Because opiates alter the sensorium, frequent assessment of level of consciousness is important. Analgesics are used in the immediate postoperative period to relieve pain and promote ventilatory excursion. Nonsteroidal anti-inflammatory drugs (NSAIDs) can increase risk of bleeding and should be used cautiously.

CARE PLANS: ABDOMINAL TRAUMA

Deficient fluid volume

Goals/outcomes

Within 12 hours of this diagnosis, patient becomes normovolemic as evidenced by mean arterial pressure (MAP) greater than 70 mm Hg, HR 60 to 100 bpm, normal sinus rhythm on ECG, central venous pressure (CVP) 2 to 6 mm Hg, PAWP 6 to 12 mm Hg, cardiac index (CI) greater than 2.5 L/min/m², SVR 900 to 1200 dynes/sec/cm⁻⁵, urinary output greater than 0.5 ml/kg/hr, warm extremities, brisk capillary refill (less than 2 seconds), and distal pulses greater than 2+ on a 0-to-4+ scale. Although hemodynamic parameters are helpful to determine adequacy of resuscitation, serum lactate and base deficit are essential to evaluate cellular perfusion.

Fluid Balance; Electrolyte and Acid-Base Balance

Fluid management

1. Monitor BP every 15 minutes, or more frequently in the presence of obvious bleeding or unstable vital signs. Be alert to changes in MAP of greater than 10 mm Hg.

Even a small but sudden decrease in BP signals the need to consult the physician, especially with the trauma patient in whom the extent of injury is unknown.

2. Monitor HR, ECG, and cardiovascular status every 15 minutes until volume is restored and vital signs are stable. Check ECG to note HR elevations and myocardial ischemic changes (i.e, ventricular dysrhythmias, ST-segment changes), which can occur because of dilutional anemia in susceptible individuals.

3. In the patient with evidence of volume depletion or active blood loss, administer pressurized fluids rapidly through several large-caliber (16-gauge or larger) catheters. Use short, large-bore IV tubing (trauma tubing) to maximize flow rate. Avoid use of stopcocks, because they slow the infusion rate.

4. Fluids should be warmed to prevent hypothermia.

HIGH ALERT!

Evaluate patency of IV catheters continuously during rapid-volume resuscitation.

5. Measure central pressures and thermodilution CO every 1 to 2 hours or more frequently if blood loss is ongoing. Calculate SVR and pulmonary vascular resistance (PVR) every 4 to 8 hours or more often in unstable patients. Be alert to low or decreasing CVP and PAWP.

HIGH ALERT!

An elevated HR, along with decreased PAWP, decreased CO/CI, and increased SVR, suggests hypovolemia (see Table 5-10 for hemodynamic profile of hypovolemic shock). Anticipate slightly elevated HR and CO caused by hyperdynamic cardiovascular state in some patients who have undergone volume resuscitation, particularly during the preoperative phase. Also anticipate mild to moderate pulmonary hypertension, especially in patients with concurrent thoracic injury, such as pulmonary contusion, smoke inhalation, or early acute respiratory distress syndrome (ARDS). ARDS is a concern in patients who have sustained major abdominal injury, inasmuch as there are many potential sources of infection and sepsis that make the development of ARDS more likely (see Acute Respiratory Distress Syndrome, p. 365).

6. Measure urinary output every 1 to 2 hours. Be alert to output less than 0.5 ml/kg/hr for 2 consecutive hours. Low urine output usually reflects inadequate intravascular volume in the patient with abdominal trauma.

7. Monitor for physical indicators of arterial hypovolemia: (1) cool extremities, (2) capillary refill greater than 2 seconds, (3) absent or decreased amplitude of distal pulses, (4) elevated serum lactate, and (5) base deficit.

8. Estimate ongoing blood loss. Measure all bloody drainage from tubes or catheters, noting drainage color (e.g., coffee grounds, burgundy, bright red [Table 3-2]). Note the frequency of dressing changes as a result of saturation with blood to estimate amount of blood loss by way of the wound site.

Table 3-2 CHARACTERISTICS OF GASTROINTESTINAL DRAINAGE

Source	Composition and Usual Character
Mouth and oropharynx	Saliva; thin, clear, watery; pH 7
Stomach	Hydrochloric acid, gastrin, pepsin, mucus; thin, brown to green, acidic
Pancreas	Enzymes and bicarbonate; thin, water, yellowish brown; alkaline
Biliary tract	Bile, including bile salts and electrolytes; bright yellow to brownish green
Duodenum	Digestive enzymes, mucus, products of digestion; thin, bright yellow to light brown, may be green, alkaline
Jejunum	Enzymes, mucus, products of digestion; brown, watery with particles
Ileum	Enzymes, mucus, digestive products, greater amounts of bacteria; brown, liquid, feculent
Colon	Digestive products, mucus, large amounts of bacteria; brown to dark brown, semiformed to firm stool
Postoperative (gastrointestinal surgery)	Initially, drainage expected to contain small amounts of fresh blood appearing bright to dark; later, drainage mixed with old blood appearing dark brown (“coffee grounds”); and then approaches normal composition
Infection present	Drainage cloudy, may be thicker than usual; strong or unusual odor, drain site often erythematous and warm

It is important to know the normal in order to recognize the abnormal.

Electrolyte Management; Fluid Monitoring; Hypovolemia Management

Acute pain

Goals/outcomes

Patient’s subjective evaluation of discomfort improves, as assessed by use of a pain scale and/or assessed by nonverbal indicators of discomfort, such as grimacing, restlessness, and/or physiologic indicators.

Pain Control; Comfort Level

Pain management

1. Medicate appropriately for pain relief. It is important to note that opiate analgesics can decrease GI motility, causing nausea, vomiting, and delay of bowel activity. These factors are especially significant if the patient has had a recent laparotomy.

2. Provide comfort measures, maintain proper positioning of affected extremities while turning patient and supporting incisional areas.

3. Explain procedures to patient and include education regarding pain relief measures.

Risk for infection

Goals/outcomes

Patient is free of infection as evidenced by core or rectal temperature less than 37.7°C (100°F); HR less than 100 bpm, CI less than 4 L/min/m²; SVR greater than 900 dynes/sec/cm⁻⁵; orientation to time, place, and person; and absence of unusual redness, warmth, or drainage at surgical incisions and drain sites.

Risk Control

Infection protection

1. Note color, character, and odor of all drainage from any surgical site, orifice, drain, or site of invasive catheters.

2. Report the presence of foul-smelling or abnormal drainage. See Table 3-2 for a description of the usual character of GI drainage.

3. Monitor temperature, hemodynamics, and vital signs closely.

Administer pneumococcal vaccine to patients with total splenectomy to minimize the risk of postsplenectomy sepsis.

4. For more interventions, see this diagnosis in Major Trauma, p. 235.

Infection Control; Infection Protection

Ineffective tissue perfusion: gastrointestinal

Goals/outcomes

Patient has adequate GI tract tissue perfusion as evidenced by normoactive bowel sounds; soft, nondistended abdomen; and return of bowel elimination.

Tissue Perfusion:

Abdominal Organs

Circulatory precautions

1. Auscultate for bowel sounds hourly during the acute phase of abdominal trauma and every 4 to 8 hours during the recovery phase. Report prolonged or sudden absence of bowel sounds during the postoperative period, because these signs may signal bowel ischemia or mesenteric infarction.

2. Evaluate patient for peritoneal signs (see Box 3-3), which may occur initially as a result of injury or may not develop until days or weeks later, if complications caused by slow bleeding or other mechanisms occur.

3. Ensure adequate intravascular volume (see Deficient Fluid Volume, p. 253).

4. Evaluate laboratory data for evidence of bleeding (e.g., serial Hct) or organ ischemia (e.g., AST, ALT, lactic dehydrogenase [LDH]). Desired values are as follows: Hct greater than 28% to 30%, AST 5 to 40 IU/L, ALT 5 to 35 IU/L, and LDH 90 to 200 U/L.

5. Document amount and character of GI secretions, drainage, and excretions.

6. Assess and report any indicators of infection or bowel obstruction (e.g., fever, severe or unusual abdominal pain, nausea and vomiting, unusual drainage from wounds or incisions, change in bowel habits).

HIGH ALERT!

Note changes that suggest bleeding (presence of frank or occult blood), infection (e.g., increased or purulent drainage), or obstruction (e.g., failure to eliminate flatus or stool within 3 to 4 days after surgery).

Circulatory Care: Arterial Insufficiency; Bowel Management

Impaired skin integrity

Goals/outcomes

Patient has adequate tissue integrity by the time of hospital discharge as evidenced by wound healing within an acceptable time frame (according to extent of injury) and absence of skin breakdown caused by GI drainage.

Tissue Integrity: Skin and Mucous Membranes

Skin surveillance

1. Protect the skin surrounding tubes, drains, or fistulas, keeping the areas clean and free from drainage. Gastric and intestinal secretions and drainage are highly irritating and can lead to skin excoriation. If necessary, apply ointments, skin barriers, or drainage pouches to protect the surrounding skin. If available, consult ostomy nurse for complex or involved cases.

2. For other interventions, see this diagnosis in Major Trauma, p. 235.

Wound Care; Tube Care

Imbalanced nutrition: less than body requirements

Goals/outcomes

Patient has adequate nutrition as evidenced by maintenance of baseline body weight and state of nitrogen balance on nitrogen studies.

Nutritional Status: Food and Fluid Intake; Nutritional Status

Nutrition management

1. Collaborate with physician, dietician, and pharmacist to estimate patient’s metabolic needs on the basis of type of injury, activity level, and nutritional status before injury.

2. Consider patient’s specific injuries when planning nutrition. For example, expect patients with hepatic or pancreatic injury to have difficulty with blood sugar regulation.

3. Patients with trauma to the upper GI tract may be fed enterally, but feeding tube must be placed distal to the injury. Disruption of the GI tract may require a feeding gastrostomy or jejunostomy. Patients with major hepatic trauma may have difficulty with protein tolerance.

4. Ensure patency of gastric or intestinal tubes to maintain decompression and encourage healing and return of bowel function. Avoid occlusion of the vent side of sump suction tubes, because this may result in vacuum occlusion of the tube.

Use caution when irrigating gastric or other tubes that have been placed in or near recently sutured organs.

• For additional information, see Nutritional Support (p. 117) and Major Trauma (p. 235).

Electrolyte Management; Feeding; Nutrition Therapy; Tube Feeding

Disturbed body image

Goals/outcomes

Patient able to acknowledge body changes, views and touches affected body part, and demonstrates movement toward incorporating changes into self-concept and able to verbalize some level of coping.

Body Image; Self-Esteem

Body image enhancement

1. Evaluate the patient’s reaction to the stoma or missing/mutilated body part by observing and noting evidence of body image disturbance (see Box 2-4).

2. Anticipate feelings of shock and disbelief initially. Be aware that trauma patients usually do not receive the emotional preparation for ostomy, amputation, and other disfiguring surgery that the patient undergoing elective surgery receives.

3. Anticipate and acknowledge normalcy of feelings of rejection and isolation (and uncleanliness in the case of fecal diversion).

4. Offer patient opportunity to view stoma/altered body part. Use mirrors if necessary.

5. Encourage patient and significant others to verbalize feelings regarding altered/missing body part.

6. Offer patient the opportunity to participate in care of ostomy, wound, or incision.

7. Confer with surgeon regarding advisability of a visit by an ostomate or a patient with similar alteration in body part.

8. Be aware that most colostomies are temporary in persons with colonic trauma. This fact can be reassuring to the patient, but it is important to verify the type of colostomy with the surgeon before explaining this to the patient.

Ostomy Care

Additional nursing diagnoses

Also see Major Trauma for Hypothermia (p. 244) and Posttrauma syndrome (p. 245). For additional information, see other diagnoses under Major Trauma, as well as nursing diagnoses and interventions in the following sections, as appropriate: Hemodynamic Monitoring (p. 75), Prolonged Immobility (p. 149), Emotional and Spiritual Support of the Patient and Significant Others (p. 200), Peritonitis (p. 805), Enterocutaneous Fistula (p. 778), SIRS, Sepsis, and MODS, (p. 924), and Acid Base Imbalances (p. 1).

Acute cardiac tamponade

Pathophysiology

Cardiac tamponade is a condition that results in a low CO state caused by decreased filling of the chambers of the heart from pressure exerted by fluid, blood, purulent liquid, or gas in the pericardial space. Cardiac tamponade is classified as acute, subacute, occult, or regional. Acute cardiac tamponade occurs when there is a rapid accumulation of fluid, which results in sudden hemodynamic instability that can be life threatening.

Potential causes of cardiac tamponade include the following:

• Trauma: blunt or penetrating cardiac trauma

• Iatrogenic: cardiac surgery, cardiac catheterization, pacemaker implant

• Nontraumatic hemorrhage: dissecting aortic aneurysm, anticoagulation therapy

• Left ventricular rupture: following extensive myocardial infarction

• Infection: viral, bacterial, or fungal

• Neoplasms/carcinoma: most commonly breast and lung

• Other: connective tissue disease, pleural effusions, radiation therapy, uremic states

Acute cardiac tamponade is usually the result of trauma, iatrogenic causes, and hemorrhage. Subacute tamponade causes are related to the slower accumulation of fluids seen with infections, neoplasms, and tissue disease. Occult or low pressure tamponade is seen in hypovolemic settings. Regional tamponade can occur with large pleural effusions or with any loculated fluid within the pericardial space. Pericardial effusions can be described using the Horowitz classification system based on the echo-free space seen with echocardiograms (Box 3-4). One must be aware that any nonacute tamponade may become acute when rapid deterioration in patient condition related to low CO occurs and requires emergent care.

Box 3-4 HOROWITZ CLASSIFICATION OF PERICARDIAL EFFUSIONS

Grade 1: Small: Echo-free space in diastole less than 10 mm

Grade 2: Moderate: Echo-free space at least greater than 10 mm posteriorly

Grade 3: Large: Echo-free space greater than 20 mm

Grade 4: Very Large: Echo-free space greater than 20 mm and compression of heart is present

Acute cardiac tamponade results in inadequate CO and decreased tissue perfusion and potential death. The rapid detection and treatment of acute tamponade are the key to patient survival. The pericardial sac contains 20 to 50 ml of fluid to protect and provide a friction-free surface for the beating heart. The pericardial sac has a fibroelastic quality, which allows limited stretching ability. A sudden addition of 50 to 100 ml of fluid can markedly increase intrapericardial pressure. Conversely, a slowly accumulating tamponade can result in 2000 ml of fluid collection without life-threatening cardiac compromise.

When there is a rapid rise in intrapericardial pressure, the heart is compressed causing a decrease in intraventricular filling. The compliance of the right side of the heart is limited, as it is competing for the fixed volume within the pericardium. The right atrium (RA) as a low pressure heart chamber is the most susceptible to collapse, which decreases filling of the right ventricle. This decreased filling results in the JVD. As the pressure continues to increase, the right ventricle (RV) has partial collapse during early diastole. The decreased RV free wall compliance causes a right-to-left shift of the septum, which is pronounced during inspiration, causing the pulsus paradoxus seen with cardiac tamponade. An unresolved tamponade puts pressure on all chambers of the heart, pulmonary vessels, and coronary arteries, causing hemodynamic instability. Hemodynamically, pulmonary artery pressures increase, an equalization of pressures of the right and left atria are seen, and decreased ventricular filling occurs. This hemodynamic compromise is the result of decreased CO and hypotension with decreased tissue perfusion.

Assessment: acute cardiac tamponade

Observation

• Early signs and symptoms: Muffled or distant heart tones, distended neck veins, hypotension (Beck triad), pulsus paradoxes, and unwillingness to lay flat/supine, anxiety, dyspnea, change in sensorium

• Early hemodynamic changes: Decreased BP, increase in RA pressure (RAP) or CVP. Pulsus paradoxus of greater than 10 mm Hg (see Box 3-2); low CO

• Late signs and symptoms: Signs of cardiogenic shock including decreased BP, weak or thready pulse, confusion, restlessness, cold clammy skin, pallor

• Late-stage hemodynamic changes: Continued hypotension, low CO, right and left atrial pressures equalize, and pulmonary artery pressure (PAP) increases

Vital signs

• Sinus tachycardia, commonly seen as compensatory response to decreased stroke volume

• Monitor BP; assess for significant hypotension, narrow pulse pressure, systolic BP less than 90, and pulsus paradoxus. Pulsus paradoxus is a drop of greater than 10 mm Hg in the systolic BP during inspiration and results from the decreased stroke volume with increased intrathoracic pressure.

• Exertional dyspnea early progressing to dyspnea and orthopnea

• Hoarseness and hiccups may be present due to laryngeal and phrenic nerve involvement.

• Low urine output is the result of low CO and taken with other signs should be viewed as a signal for intervention in the absence of hemodynamic monitoring.

Auscultation

• Beck triad of muffled or distant heart tones, distended neck veins, and hypotension, although described as classic, are seen in 10% to 33% of patients. Muffled heart tones may not be apparent with the patient sitting upright, depending on the volume of tamponade. JVD is not always present in acute tamponade, as it is commonly seen in constrictive pericarditis. In the presence of hypovolemia, blood flowing toward the RA during inspiration makes the finding of JVD less likely. Pericardial friction rub may be heard with pericarditis.

Percussion

• Dullness to percussion under the left scapula posteriorly, related to compression of the left lower lobe, Bamberger-Pins-Ewart sign

Hemodynamic monitoring

If hemodynamic monitoring is not already in progress, do not delay other treatments, but prepare for appropriate monitoring, according to the hemodynamic system used. This may include insertion and monitoring of an arterial line and pulmonary artery catheter or another system capable of cardiac output measurement.

• Decreased BP: SBP less than 90 mm Hg requires intervention

• Increased CVP: Greater than 12 mm Hg

• Pulsus paradoxus: Greater than 10 mm Hg; easily seen in arterial waveform with lower systolic BP during inspiration

• Absence of Kussmaul sign: Kussmaul sign is the absence of a decline in jugular venous pressure during inspiration. Because the RV can accommodate increased volume with inspiration in tamponade, a decline in the jugular venous pressure can be seen. This is significant as to differentiate tamponade from constrictive pericarditis.

• Low CO: CI less than 2.2

• Pulmonary artery pressure (PAP): Increased

• CVP equalizes with left atrial pressure (LAP) or pulmonary artery occlusive pressure (PAOP).

• BP, CO, and CI continue to decrease, requiring fluid and vasopressor and inotropic support until definitive treatment is provided.

• If untreated, tamponade can lead to PEA or total cardiac arrest.

Abnormally elevated CVP, PAP, and pulsus paradoxus may not be seen with hypovolemic patient until fluid administration is begun.

• Pulsus paradoxus related to hypovolemia will resolve with fluid administration.

• Pulsus paradoxus will not resolve in acute cardiac tamponade with fluid administration alone.

Screening diagnostic tests

• Echocardiogram is indicated as a quick diagnostic tool for assessment.

Diagnostic Tests for Acute Cardiac Tamponade
Test	Purpose	Abnormal Findings

Electrocardiogram (ECG): 12 lead	Assess for any ischemia or infarct, underlying rhythm disturbances, or pericarditis.	Electrical alternans is a beat-to-beat change in the QRS, from swinging of the heart within the pericardium. It is rare and seen with very large volume effusions. Presence of ST-segment depression or T-wave inversion (myocardial ischemia), ST elevation (acute myocardial infarction), new bundle branch block (especially left bundle branch block), or pathologic Q waves (resolving/resolved myocardial infarction) in two contiguous or related leads. Pericarditis shows ST-segment and T-wave changes, which are often confused with ischemic changes but are more diffuse and follow a four-stage pattern (Table 5-9). Low voltage of QRS highly indicative of tamponade
*Radiology*
Chest radiograph (CXR)	Assess for a widening mediastinum. Assess size of heart, thoracic cage (for fractures), thoracic aorta (for aneurysm), and lungs (pneumonia, pneumothorax); assists with differential diagnosis of chest pain.	Widening mediastinum is indicative of acute cardiac tamponade, especially important for trauma, postprocedural, and postsurgical patients. Cardiac silhouette enlargement with clear lung fields is indicative of pericardial effusion; but >200 ml of fluid must be present for this finding to be apparent.
Echocardiography (2D or Doppler ECHO)	It is the most definitive test for diagnosing early cardiac tamponade. Assessment of thoracic aneurysms that might have dissected into the valve or coronary arteries causing tamponade. Determine type of fluid within the pericardial space. Assess for mechanical abnormalities related to effective pumping of blood from both sides of the heart.	Pericardial effusions with and without tamponade. Aortic dissections and aneurysms. Abnormal ventricular wall movement or motion, low ejection fraction, incompetent or stenosed heart valves, abnormal intracardiac chamber pressures
Transesophageal ECHO	Post cardiac surgery effusions often accumulate at the posterior wall with compression of RA. Useful for assessment of regional cardiac tamponade. Also can be done without delay while patient is being prepped in operating room for emergent thoracotomy or can be done in operating room. Assess for mechanical abnormalities related to ineffective pumping of blood from both sides of the heart using a transducer attached to an endoscope.	Same as above but can provide enhanced views, particularly of the posterior wall of the heart.
*Blood Studies*
Complete blood count (CBC) Hemoglobin (Hgb) Hematocrit (Hct) RBC count (RBCs) WBC count (WBCs) Erythrocyte sedimentation rate (ESR)	Assess for anemia, inflammation, and infection; assists with differential diagnosis of cause of tamponade.	Decreased RBCs, Hgb, or Hct reflects hemorrhage or anemia. Elevated WBC and or ESR indicative of infection or inflammatory pericarditis unless secondary to uremia.
Coagulation profile Prothrombin time (PT) with international normalized ratio (INR) Partial thromboplastin time (PTT) Fibrinogen D-dimer	Assess for causes of bleeding, clotting, and disseminated intravascular coagulation (DIC) indicative of abnormal clotting present in shock or ensuing shock. Anticoagulated patients are at higher risk for tamponade with procedures.	Elevated PTT, PT with high INR promotes bleeding; elevated fibrinogen and D-dimer reflect abnormal clotting is present.
Electrolytes Potassium (K⁺) Magnesium (Mg²⁺) Calcium (Ca²⁺) Sodium (Na⁺)	Assess for possible causes of dysrhythmias and/or heart failure.	Decrease in K⁺, Mg²⁺, or Ca²⁺ may cause dysrhythmias. Elevation of Na⁺ may indicate dehydration (blood is more coagulable). Low Na⁺ may indicate fluid retention and/or heart failure.
Other C-reactive protein (CRP) Anti–streptolysin O (ASO)	Assess for cause of pericarditis.	CRP can be indicative of inflammation unless patient has uremia. ASO elevated with immunologic cause.

Collaborative management

Guidelines on the Diagnosis and Management of Pericardial Disease from the Task Force on the Diagnosis and Management of Pericardial Diseases of the European Society of Cardiology
In 2004, findings were published from the Task Force on the Diagnosis and Management of Pericardial Diseases in the European Heart Journal. These findings included specific recommendations for various forms of pericardial disease to include cardiac tamponade. The treatment guidelines have been widely cited in the worldwide medical literature. The following are limited to the recommendations for the treatment of acute (surgical) cardiac tamponade.
Intervention	Rationale
The diagnostic tests as presented reflect these guidelines with the addition of CT, spin-echo, and cine MRI.	To assess the size and extent of simple and complex pericardial effusions. These are also helpful to measure the size of very large effusions.
Pericardiocentesis (Class I)	Absolute indication for cardiac tamponade with hemodynamic instability
Surgical drainage with bleeding suppression (Class I)	For wounds, ruptured ventricular aneurysm, or dissecting aorta aneurysm with hemorrhage or any tamponade in which needle clotting would make needle evacuation impossible
Thoracoscopic drainage, subxiphoid window, or open surgery	Indicated for loculated tamponade
In 2003, the American College of Cardiology (ACC), the American Heart Association (AHA), and the American Society of Echocardiography (ASE) presented a task force recommendation for the use of echocardiography for all patients with pericardial disease. This recommendation would include the cardiac tamponade patient unless an emergent surgical procedure was needed prior to evaluation.

From www.acc.org/qualityandscience/clinical/statements.htm

Care priorities

1. Stabilize ventilation with oxygen, intubation, and mechanical ventilation:

Oxygen is administered using the equipment that most effectively corrects each patient’s hypoxia. Devices used range from nasal cannula to 100% nonrebreather masks to mechanical ventilators. If patient presented in cardiac arrest, chest compressions may be in progress while ventilation is being stabilized.

2. Facilitate providing pericardiocentesis:

Needle aspiration of the pericardium can be performed using a subxiphoid or left parasternal approach to drain excess fluid from the pericardial space. The blood removed often will not clot, since the heart action can cause clotting factors within the pericardial sac to break down (defibrination). Pericardiocentesis alone may not suffice to manage acute pericardial tamponade. Surgical exploration with pericardial window is recommended because of the high incidence of recurrent bleeding if surgery is not performed. A drain may stay in place until fluid output decreases or ceases.

3. Anticipate the need to provide a surgical procedure:

Subxiphoid pericardiostomy is a resection of the xiphoid process to drain the pericardial sac. It is performed using either local or general anesthesia. Other, more extensive surgical procedures, including a pericardiectomy, can be used for cardiac decompression. An immediate thoracotomy can be done in the ICU or emergency department if the patient becomes suddenly bradycardic (HR less than 50 bpm) or severely hypotensive (systolic BP less than 70 mm Hg) or has a PEA or cardiac arrest. Thoracotomy allows for pericardial sac evacuation, hemorrhage control, and internal cardiac massage if needed.

4. Provide fluid resuscitation:

IV fluid infusion is used to increase ventricular filling pressures during diastole and may result in increased CO and BP. Blood products, colloids, or crystalloids may be used.

5. Administer vasopressors:

Medications used to increase the BP by stimulating vasoconstriction in the peripheral vasculature include neosynephrine or norepinephrine. These medications are less effective in a setting of hypovolemia.

6. Administer inotropic agents:

Medications used to increase myocardial contractility and CO include dopamine, dobutamine, and milrinone (see Appendix 6).

7. Stabilize bp with ongoing titration of medications and fluids:

This must be done with hemodynamic monitoring and goal-directed therapy derived at by the entire critical care team.

CARE PLANS: ACUTE CARDIAC TAMPONADE

Decreased cardiac output (co)

Goals/outcomes

Within 4 to 6 hours after fluid resuscitation or evacuation of tamponade, patient has adequate CO as evidenced by CVP 4–6 mm Hg, CO 4 to 7 L/min, CI ≥2.5 L/min, systolic BP at least 90 mm Hg (or within patient’s normal range), HR 60 to 100 bpm, normal sinus rhythm on ECG, and absence of new murmurs or gallops, distended neck veins, and pulsus paradoxus.

Cardiac Pump Effectiveness

Cardiac care: acute hemodynamic regulation

1. Assess cardiovascular function by evaluating heart sounds and neck veins hourly. Consult physician for muffled heart sounds, new murmurs, new gallops, irregularities in rate and rhythm, and distended neck veins.

2. Monitor all patients with blunt or penetrating trauma to the chest and abdomen for physical signs of acute cardiac tamponade, persistent hemodynamic instability, and shock symptoms more severe than expected for the blood loss.

3. Evaluate patient for pulsus paradoxus: an abnormal decrease in arterial systolic BP during inspiration compared with that during expiration of greater than 10 mm Hg difference (see Box 3-2).

4. Measure and record hemodynamic parameters. Consult physician or midlevel practitioner for sudden abnormalities or changes in trend. Early signs of tamponade include elevated CVP with normal BP and pulsus paradoxus. Later signs include equalization of CVP and LAP (PAOP) and elevated PAP in the presence of hypotension and low CO and CI (see Box 3-4).

5. Evaluate ECG for ST-segment changes, T-wave changes, rate, and rhythm. The optimum is sinus rhythm or sinus tachycardia. Maintain continuous cardiac monitoring.

6. For patients presenting with PEA and narrow-complex tachycardia on ECG, have a high suspicion of acute cardiac tamponade as the cause and follow ACLS guidelines.

7. Administer blood products, colloids, or crystalloids as prescribed. For trauma patients, use large-bore IV lines in the periphery, if possible. Use pressure infusers and rapid-volume/warmer infusers for patients who require massive fluid resuscitation.

8. Be prepared to administer vasopressor agents (e.g., norepinephrine, phenylephrine, dopamine) if fluid resuscitation does not support patient’s BP. Positive isotropic agents (e.g., milrinone) may be used to support CO in short-term management. The underlying problem is decreased ventricular filling, so these are temporizing measures for hemodynamic support until correction of the tamponade occurs.

9. Have emergency equipment available for immediate pulmonary artery catheterization, central line insertion, arterial line insertion, pericardiocentesis, or thoracotomy.

10. Assess heart rate and monitor ECG: sinus tachycardia, commonly seen as compensatory response to decreased stroke volume.

Cardiac Care; Cardiac Care: Acute; Emergency Care; Hemodynamic Regulation; Invasive Hemodynamic Monitoring; Fluid Monitoring; Fluid Management; Blood Product Administration; Medication Administration; Oxygen Therapy; Resuscitation; Shock Management: Cardiac; Vital Signs Monitoring; Dysrhythmia Management

Ineffective tissue perfusion: pulmonary, peripheral, and cerebral

Goals/outcomes

Within 4 to 6 hours after management with fluids or evacuation of tamponade, patient has adequate perfusion as evidenced by orientation to time, place, and person; systolic BP at least 90 mm Hg (or within patient’s normal range); RR 12 to 20 breaths/min with normal depth and pattern (eupnea) and ease of respirations; SaO₂ at least 95%; peripheral pulses at least 2+ on a 0-to-4+ scale; equal and normoreactive pupils; warm and dry skin; brisk capillary refill (less than 2 seconds); and urine output at least 0.5 ml/kg/hr.

Circulation Status

Shock management: cardiac

1. Assess tissue perfusion by evaluating the following at least hourly: level of consciousness (LOC), BP, pulses, pupillary response, skin temperature, and capillary refill.

2. Evaluate urine output hourly to ensure that it is at least 0.5 ml/kg/hr.

3. Maintain tissue perfusion by delivering prescribed blood products, colloids, crystalloids, vasopressors, and positive inotropes.

4. If hypotension occurs: ensure hypovolemia is treated, with fluid administration, prior to or simultaneously with vasopressors for treatment of hypotension. Administer vasopressors via central line whenever possible. Frequently assess peripheral IV lines for evidence of infiltration. If vasopressor agents infiltrate subcutaneous tissues, necrosis occurs. Follow appropriate management protocol for your institution.

5. Have emergency oxygen and intubation and mechanical ventilation equipment available.

6. Anticipate and prepare for emergent surgery and pericardiocentesis evacuation, if needed.

Vasopressors (e.g., norepinephrine, phenylephrine, dopamine) should be infused through a central line.

Cardiac Care: Acute; Circulatory Care; Emergency Care; Invasive Hemodynamic Monitoring; Respiratory Monitoring; Shock Management; Vital Signs Monitoring; Cerebral Perfusion Promotion; Neurologic Monitoring; Medication Administration; Medication Management; Oxygen Therapy; Intravenous Therapy; Fluid/Electrolyte Management

Injury to the spinal cord can be a devastating event initiating a cascade of physical and psychological changes that may last a lifetime. Spinal cord injury (SCI) affects 7800 to 10,000 people each year. The average age at injury is 37.6 years; this number depicts an increasing trend across all injury categories (MVCs, sports, and falls). The rising trend reflects an increase in the number of injuries in those who are 60 years and older. Female injuries now account for 21.8% of new SCIs, but young white males continue to lead the injury profile. Cervical injuries occur most frequently at a rate of 56% over lumbar and thoracic injuries. MVCs cause 44% of injuries, followed by acts of violence (24%), falls (22%), sports injuries (8%), and other causes (2%). Persons living with an SCI are estimated as between 250,000 and 400,000, and approximately 85% of SCI patients who survive the initial 24 hours live at least 10 years.

The spinal cord is approximately 18 inches in length running from the base of the brain to the lumbar (L) spine area between L1-2 where the cord tapers to form the conus medullaris, a bulbous end that terminates into a collection of nerve roots known as the cauda equina (horse’s tail). The spinal nerve roots exit the spinal cord at corresponding levels below the vertebral body of the spinal column and are the anatomical connection between the central and peripheral nervous system. Since the spinal cord ends at L1-2, the nerves descending from the conus medullaris making up the cauda equina are considered peripheral nerves. The brain and spinal cord communicate sensory and motor information along a complex system of tracts, some descending from the brain (motor) and others ascending from the periphery (sensory). Damage to pathways along this communication system results in unique but quite distinguishable syndromes that include upper motor neurons (UMNs), which carry messages between the brain and the periphery along the spinal cord, and lower motor neurons (LMNs), those nerves that branch out from the vertebrae (peripheral nerves). Damage to UMNs results in muscle spasticity and hyperreflexia, while damage to LMNs results in muscle flaccidity and areflexia.

Mechanisms of injury to the spinal cord can be traumatic or nontraumatic. Traumatic injuries include MVCs, falls, sports injuries, or acts of violence (e.g., gunshot wounds or stabbings). These injuries are the result of mechanical forces that result in sudden flexion, hyperextension, vertebral fracture, compression of the cord, rotation of the cord, or direct injury to the cord as in a stabbing or gunshot wound. Nontraumatic injuries may be a result of vascular injury (aortic disruption or spinal artery occlusion), degenerative diseases (spondylosis), inflammatory events, neoplasms, or autoimmune diseases (multiple sclerosis). Injuries to the spinal cord regardless of mechanism of injury include concussion, contusion, laceration, transsection, hemorrhage, ischemia, and avascularization. See SCI classifications and terminology in Table 3-3.

Table 3-3 SPINAL CORD INJURY CLASSIFICATIONS AND TERMINOLOGY

Type	Closed (blunt) Open (gunshot wound or stabbing)
Cause	Motor vehicle crashes, falls, sports-related injury, acts of violence
Site	Level of injury involved (cervical thoracic, lumbar, sacral)
Mechanism	Flexion (deceleration injury, backward fall, diving injury) Extension (whiplash or fall with hyperextension of neck)
Stability	Integrity of supporting anatomy including vertebral bodies, ligaments, articulating processes, and facet joints
Complete	Tetraplegia (quadraplegia) or paraplegia (absence of motor, sensory, and vasomotor function below the level of the injury) More frequently seen in cervical injuries
Incomplete	Sparing of some motor and sensory function below the level of the lesion More frequently seen in lumbar injuries

Fractures involving the vertebral bodies

These fractures may or may not cause SCI. Severe SCI can occur without damage to the vertebrae. With severe fractures, such as the “burst” fracture (fragmentation of a vertebral body with penetration of the spinal cord), paralysis almost always occurs. Penetration of the spinal cord with bony fragments may cause hemorrhage, infection, and leakage of cerebrospinal fluid (CSF).

Spinal shock

Spinal shock occurs following both complete and partial transsection of the cord. It is a temporary loss of reflex function in all segments below the level of injury that occurs immediately after SCI, lasting several hours to weeks.

Neurogenic shock

Neurogenic shock occurs in patients who injure the cervical or upper thoracic cord, disrupting sympathetic innervation to the vasculature, and the heart is impaired, causing dilation of blood vessels and bradycardia, often causing hypotension. The loss of sympathetic innervation also causes venous pooling in the extremities and splanchnic vasculature. Venous return to the heart is decreased, resulting in decreased CO and poor tissue perfusion.

Spinal shock with neurogenic shock

Patients who injure the cervical or upper thoracic cord may experience neurogenic shock and spinal shock simultaneously.

Although spinal shock is seen in SCIs at any level, the loss of central control of peripheral vascular tone (neurogenic shock) occurs most dramatically in high cervical spine injuries, with interruption of the sympathetic nervous system. Profound bradycardia and hypotension are possible. With SCIs lower than the midthoracic area, the patient will experience a phase of neurogenic shock, with loss of sympathetic innervation to vasculature below the level of the lesion; however, the effects of that loss are not as dramatic.

Autonomic dysreflexia

A life-threatening condition affecting victims with lesions at or above T6, stemming from stimulation of the SNS by relatively minor events. The resultant uncompensated cardiovascular response may cause seizures, subarachnoid hemorrhage, fatal cerebrovascular accident, and myocardial infarction if not immediately recognized and treated. Once spinal shock resolves, autonomic dysreflexia (AD) may occur at any time from the acute phase to several years following the injury.

Causes:

Most commonly, stimuli to the bladder, including distention, infection, calculi, cystoscopy; or from the bowel with fecal impaction, rectal examination, suppository insertion; or from the skin, such as tight clothing or sheets, temperature extremes, sores, or areas of broken skin.

• Flaccid paralysis below the level of injury of all skeletal muscles with absence of deep tendon reflexes (DTRs)

• Loss of cutaneous sensation

• Loss of temperature control with development of anhidrosis (absence of sweating)

• Loss of vasomotor tone

• Loss of proprioception (position sense)

• Loss of visceral and somatic sensation, and loss of the penile reflex

• Bowel and bladder paralysis resulting in urinary retention and fecal retention occurring along with GI shutdown resulting in paralytic ileus

Recovery phase of spinal shock

As spinal shock subsides, the patient may experience:

• Flexor spasms evoked by cutaneous stimulation

• Reflex emptying of the bowel and bladder

• Extensor or flexor rigidity

• Hyperreflexic DTRs, and reflex priapism or ejaculation in the male, evoked by cutaneous stimulation.

Autonomic dysreflexia

Symptoms include:

Table 3-4 LEVELS OF CORD INJURY

Level of Injury	Manifestation
C4 and above	Loss of muscle function, including respiratory function; fatal outcome unless ventilation is provided immediately
C4-C5	Same as above; phrenic nerve may be spared; assisted ventilation; quadriplegia/tetraplegia
C6-C8	Diaphragm and accessory muscles or respiration retained; movement of neck, shoulders, chest, and upper arms; quadriplegia
T1-T3	Neck, chest, shoulder, arm, hand, and respiratory function retained; difficulty maintaining a sitting position; paraplegia
T4-T10	More stability of trunk muscles; paraplegia
T11-L2	Use of upper extremities, neck, and shoulders; some function of upper thigh; reflex emptying of bowel; males may have difficulty achieving and maintaining an erection; decreased seminal emission
L3-S1	Reflex emptying of bowel/bladder; decreased/lack of ability to have an erection; decreased seminal emission; all muscle groups in upper body function; most muscles of lower extremities function
S2-S4	Flaccid bowel and bladder; lower extremity weakness; all muscle groups function; no ability to have a reflex erection