Trauma

1.All patients are full stomachs

• 2.Partial airway obstruction can rapidly
• advance to complete airway obstruction.

3.All patients are hypovolemic.

• 4.All patients have a cervical spine injury
• until proven otherwise

1.CNS function

• 2.Maintaining adequate respiratory gas
• exchange.

3.Achieving circulatory homeostasis

• Primary
• and Secondary surveys

Primary

• –The ABCDEs of trauma.  Airway, Breathing, Circulation, Disability,
• and Exposure

• –Immediate response by trauma or team
• using ACLS and ATLS protocols

• –Controlling of hemorrhage and repair of
• definitive repair of injury are two phases that are part of the resuscitation
• phase

secondary surveys are done to rule out occult injuries

Brain death in 5-10 min if without oxygen

•Oxygenation and prevent aspiration

• •Assume cervical spine injury (even if
• injury is below clavicle)

•Use jaw thrust maneuver

• •In- line stabilization with assistance.
• (prevent neck flexion, extension and rotation)

• •C1-C2 injuries may require nasal
• intubation

•Use oral and nasal airways.  Goal is to prevent neck extension

• •CT scan is best method for ruling out
• cervical fracture for all C spine vertebrae

• •Trauma patients are always at risk for
• aspiration

• •Use non particulate antacids into the
• stomach, H2 antagonists and reglan to raise ph and reduce volume of gastric contents .5
• to 1 hr before intubation (ensuring adequate
• oxygenation by ensuring ability to ventilate outweighs the risk of aspiration
• pneumonia)

Indications:

1.Cardiac or respiratory arrest

2.Respiratory insufficiency

3.Airway protection

4.Need for deep sedation or analgesia (burns), up to including general anesthesia

• 5.Transient hyperventilation of patients with space occupying lesions and evidence of
• increased ICP

6.Delivery of 100% FIO2 to patients with CO poisoning

7.Facilitation of the diagnostic workup in uncooperative or intoxicated patients

•Technically challenging  for inexperienced anesthesia providers

• • Studies show high incidence of airway
• complications and aspiration associated with nasal intubation

•  A well performed oral laryngoscopy with inline stabilization can be performed without spinal cord damage

• Do not perform nasal intubation in patients with mid face or basilar skull fractures

• •If patient presents with an esophageal obturator airway, leave it until trachea is
• intubated due to risk of regurgitation

Awake fiberoptic intubation

DL with 6cm ETT or smaller

Trach

Cricothyrotomy

• If facial or neck injuries preclude visualization of the laryxn or if there is acute obstruction
• of the upper airway

• Fiberoptic or awake intubation use local
• anesthesia

• 
• 

1.Awake fiberoptic intubation

• 2.Direct laryngoscopy with 6cm ETT (or
• smaller)

3.Tracheostomy

4.Cricothyrotomy

• If facial or neck injuries preclude
• visualization of larynx, or if there is acute obstruction of upper airway.

üFiberoptic or awake intubation use local anesthesia and antisialogogues.

Patients with massive disruption of the floor of the mouth

Disruption of the larynx or cervical trachea:

• •Assist or mechanical ventilation with
• bag-valve mask or mechanical ventilator

• •Deliver 100% O2 until blood gas is
• obtained

• •If patient arrives intubated, confirm
• placement

• •Hyperventilate suspected head trauma
• patients. (decreases ICP)

•Conditions compromising ventilation:

• Flail chest, obstruction of the
• endotracheal tube, or direct pulmonary injury

• •Shock—denotes circulatory failure leading
• to impaired end organ perfusion and oxygen delivery

• •In trauma, shock is mainly a result of hypovolemia (shock is due to hemorrhage until proven
• otherwise)

•Hemorrhage-- responses include tachycardia, decrease pulse pressure, hypotension, tachypnea, and delirium

• HCT and Hgb are often not accurate indicators of acute blood loss

• •Massive tissue damage and peripheral
• somatic nerve stimulation exacerbate the reductions in cardiac output and
• stroke volume seen in hypovolemic shock

•Trauma patients require A-line monitoring

• • The degree of hypotension on presentation
• to the ER and the OR correlates strongly with mortality

•Multiple large bore IV catheters.  (at least two 16 g PIVs)

•Place Ivs in superior and inferior caval systems

•GCS score

•Evaluate central function

1.Alert

2.Responds to vocal stimulus

3.Responds to painful stimulus

4.Unresponsive

•Full motor and sensory exam

• •Cervical spine films. Head, neck, and
• spine CT

• •Assess for possible immediate surgery,
• ICP monitoring, support of vital functions

•Removal of all clothing and assessing for any occult injuries

•Lab studies, ECG, CT scans and X-rays

•Detailed history and complete physical exam

•Evaluate for surgical treatment if necessary (immediate or delayed)

•Review of all findings

•Evaluate potential for systemic infection (sepsis is a leading cause of complications and death in trauma patients)

• •Do not delay wound treatment and treatment of open fractures if possible. (some
• radiographic and laboratory exams can wait)

•Determine with team which surgery should be prioritized

• •One third of 150,000 deaths in the U.S. due to trauma result from fatal head
• injuries

•25% of the 1 million survivors of TBI require inpatient care ( many of the survivors are more impaired than survivors of non TBI trauma.)

•Trauma patients with altered consciousness should be considered to have brain injury

•Brain injury -- evidenced by restlessness, convulsions and cranial nerve dysfunction (non reactive pupil)

•Cushings triad ( hypertension, altered breathing pattern, bradycardia )is a late and unreliable sign and just precedes brain herniation

•Hold sedatives and anticholinergics prior to initial neuro assessment

GCS 13-15.

•Most common and usually requires observation and radiologic exam. Elderly patients may exhibit a honeymoon syndrome

•If GCS is normal after 24 hours, deterioration is unlikely

•Mild TBI patients may exhibit post-concussive symptoms: headache, memory loss, emotional lability, and sleep disturbance

GCS 9-12.  Higher potential for deterioration.  Immediate CT.

•Early intubation, mechanical ventilation, and close observation

•Patients may be combative, agitated, risk for aspiration and hemodynamic decline.

•Need to be stabilized. Follow CT scans and repeat if changes occur

•Assess for need of ICP monitoring

•Timing of early surgical intervention?

•GCS of 8 or less on admission

•High risk for mortality

• •Early, rapid management focused on restoration of systemic homeostasis and
• perfusion-directed care of  the injured brain

•Rapid airway management—Episode of PO2 , 60 mm Hg doubles mortality

•Many patients arrive intubated due to new protocols  (oxygenate by whatever means possible)

•PEEP? Hypocapnea? 

• •CBF decreases after TBI. (vasoreactivity is
• not always intact in TBI)

•Maintain PaCO2 at 35 mmHg, unless ICP can’t be controlled with barbiturates, sedatives, CSF drainage, NM blockade, and osmotic agents

•A single episode of hypotension (SBP < 90 mmHg) is associated with an increase in morbidity and a doubling of mortality after TBI

• •Severe TBI patients should be maintained with SBP> 110 with a MAP >90 for goal
• pressures

•American Association for Neurological Surgeons (AANS) and the Brain Trauma Foundation suggest guidelines where severe TBI patients should be have a CPP maintained at 70 mm Hg at all times

• •Fluid therapy followed by vasoactive therapy are mainstays in the management of these
• patients (euvolemic state)

• •Severe head trauma may result in
• pulmonary shunting and V/Q mismatch. 
• (atelectasis, aspiration, or direct neural defect on pulmonary vasculature

• •Increase ICP may predispose patients to
• pulmonary edema because of sympathetic 
• outflow

•Ideal ICP threshold—not universally defined

•Patients have been know to herniate at ICP 20 mmHg or lower so ICP level is individualized

•ICP monitoring indicated for patients with severe head injury (GCS <8), and abnormal head CT findings (hematoma, contusions, edema, or compressed basal cisterns)

•Positional therapy-elevate patient’s head to facilitate venous drainage; moves CSF to spinal canal. May improve oxygenation due to improved VQ

•Analgesics– Pain will increase CMRO2

•Sedatives—Propofol ( in addition to a narcotic) has been shown to maintain ICP in TBI patients without the use of additional use of CNS depressant agents and NM blockers

Decompressive craniectomy:

• •Used to control severely elevated ICP and prevent herniation and stroke.  May reduce morbidity and mortality in
• patients who may not otherwise survive.

• Hypothermia: •Once believed to reduce rate of cerebral edema and mortality after cortical injury.  Recent studies show no improvement in outcomes after maintenance of moderate
• hypothermia (33 C)for 24 –48 hrs.(hyperthermia can increase CMRO2)

• •Mannitiol–
• reduces ICP through it’s action as an osmotic diuretic and a cerebral arteriolar vasoconstrictor.  (may cause rebound increase in ICP in patients who are not euvolemic),

• Hypertonic saline:
• •Osmotic effect on edematous cerebral tissue, vasodilatory actions, attenuates excitatory neurotransmitters after TBI (due to
• perturbations of extracellular sodium), and depresses leukocyte adherence and neutrophil migration (may offer protection from bacterial illnesses)

Barbiturate coma:

•Lowers CMRO2, decrease excitatory neurotransmitters (glutamate,lactate, aspartate).  Barbiturate coma is considered when interventions previously mentioned are ineffective.

• •Essential to have strict management of intravascular volume and may necessitate PA
• catheterization and frequent use of vasoactive agents. (a-line).

•Spinal cord injury 4:1 males to female

•11,00 new US cases per year.

•Early mortality is 50%, while <10 % improve neurologically.

•Early intervention and prevention of further spinal injury is crucial.

•Degree is proportional to the level of the lesion

• •May involve phrenic nerves C3-C5 and
• cause apnea.

•Loss of intercostals function limits pulmonary reserve and ability to clear airway.

• •Injuries at T1-T4 eliminate sympathetic
• innervation of the heart –bradycardia.

• •Acute high spinal cord injuries may lead
• to spinal shock.

• •Spinal shock is the loss of sympathetic
• vasomotor tone below the level of injury—hypotension, bradycardia, areflexia, and gastrointestinal atony. 

Look for venous distension in the legs. May require aggressive fluid therapy in the initial phases of spinal shock. 

•Shock occurs form disruption of sympathetic outflow from T1-L2 which results in unopposed vagal tone and vasodilation and pooling of blood in vascular beds

• • Some CV abnormalities include bradycardia < 45 bpm in 71% of cases. ( usually resolves in 2-3 weeks)  May also be triggered by
• turning, suctioning or any other stimulation

Hyperventilation may induce hyperemia in area of the brain that may not have intact auto regulatory mechanisms

• •Hypotension defined as SBP < 90mmHg or
• 30% below baseline in 68% of cases

•High cervical injuries necessitate invasive monitoring.  Paop(occlusive) pressures of 14-18 appear to be of benefit to SCI patient

•Monitor of arrhythmias; SVT, bradycardia, systole, ventricular arrhythmias, atrial fibrillation

Cardiac arrest in 16% of cases

•Fiberoptic placement of ETT is preferred route in the OR (controlled setting)

•Emergentintubation of trachea with DL and in-line stabilization is acceptable (ER)

• •Proper oxygenation and fluid resuscitation and minimization of secondary injury to
• neural tissue

•Supportive cardiac and respiratory therapy to counteract vasodilation and hypoventilation

•Succinylcholine is reportedly safe during the first 48 hours following an injury but is associated with life threatening hyperkalemia afterward

• •High dose corticosteroid therapy with
• methylprednisolone (30mg/kg followed by 5.4 mg/kg hour for 23 hours improves
• neurologic outcome of patients with spinal cord trauma. (small but statistically significant improvements)

•Autonomic hyperreflexia is associated with lesions above T5 but is not a problem during acute management

• •Beware of electrolyte disturbances:
• hyperkalemia, hypercalcemia, hyperphosphatemia, hyponatremia

• •Associated injuries: spine, thoracic,
• intracranial, intra-abdominal bleeding and myocardial contusion.

•Check for Trismus, which is lock jaw  (as a result of injury)

•LeFort I:  Transverse.  The body of the maxilla is separated from the base of the skull above the level of the palate and below the level of the zygomatic process

•LeFort II: Pryamidal. Vertical fractures through the facial aspects of the maxilla extend upward through the nasal and ethmoid bones

• •Type III: Craniofacial dysjunction. 
• Fractures extend through the frontozygomatic suture lines bilaterally, across the orbits, and through the base of the nose and the ethmoid region

•Cerebrospinal fluid rhinnorrhea –( avoid nasal airway nasogastric tubes  Positive pressure ventilation can potentially cause pneumocephalus)

1. Poor movement of jaw, swelling, and broken  teeth

• 2. Posterior displacement of tongue (
• airway obstruction)  associated with condylar or parasymphaseal fractures of the mandible.  Simple forward traction of the tongue often
• provides relief.

• 3. Maxillary fixation and occlusion may
• necessitate nasal intubation if not otherwise contraindicated  (Severely busted nose)
• LeFort Fracture II and III

•May require deep anesthesia and complete paralysis

•Caution to prevent large swings in BP. Intraoccular pressure and perfusion

•Prevent coughing from ETT

• •Nasal intubations are contraindicated
• with basilar skull fractures and mid face fractures

• •Mask ventilation is frequently impossible
• in the setting of severe facial deformity, excessive intraoral bleeding, or
• basilar skull fractures

• •Postoperative intramaxillary fixation and nasal packing may make it
• impossible to reintubate patient

• •Patient may require relatively short term
• tracheotomy

• •Beware of associated cervical spine
• injuries

• •Fevers often exist in patients with panfacial fractures ( rule out MH by lack of
• metabolic or respiratory acidosis)

• •Consider location of injury for airway
• management

• •Beware of partial airway obstruction
• (hematoma and edema may expand during 6-12 hours after injury)

• •Caution with fluid administration due to
• risk of airway edema

• •Deep anesthesia with prevention of
• patient moving or coughing

• •Consider prolonged intubation and airway
• management

• •Cervical spine injury, esophageal injury,
• injury to major vessels, and airway.

•Danger of expanding hematoma  (remember precepts).

•Caution not to dislodge clot with a “light induction” (proceed with caution in setting of airway injury)

•Diagnosis of penetrating injury to larynx is made by the presence of air bubbling through the penetration tract, hoarseness or dysphonia, flattening of thyroid cartilage protuberance.

• •May need to intubate a penetrated wound
• (gunshot or stab wound to lower airway)

• •Clothesline injury-
• result in the avulsion of the larynx from the trachea and separation between the cricoid cartilage and the first tracheal ring.  (not always presented as an open wound).

• •Intimal disruption of carotid arteries from blunt trauma. (may result in dissection without immediate symptoms.  (may require
• ultrasound or angiography to rule out such injury)

• Penetrating trauma—compression to occlude bleeding vessels and prevent air embolism. Keep patient flat or slightly head down.  Positive pressure ventilation is used to increase venous pressure of neck.

• • Assess for upper thoracic and upper
• great vessel injury form lower neck trauma

• •Anesthetic management;  Secure airway manually or surgically. 
• Consider peripheral access due to potential injury to great vessels

• Direct effect on:

1. Cardiopulmonary system

2. Effects from shock state

3. CNS effects from air embolism.

•Traumatic thoracic aortic dissection or aneurysm  (Immediate surgical intervention.)  Dx’d by widened mediastinum on an upright roentgenogram prior to arteriographic conformation

• •Blunt chest trauma with pulmonary
• lacerations and air leaks, and hemorrhage (surgical correction)

•Hemopericardium or pneumopericardium requires immediate pericardiocentesis to relieve tamponade followed by a pericardial window to prevent reaccumulation

•Traumatic lacerations of the heart are either rapidly fatal or slow enough to allow for time to surgically repair them

• •Rib fractures may continually allow for
• air to enter vascular spaces

• •Consider continuous regional anesthesia
• for the patient recovering from multiple rib fractures; reduces respiratory
• compromise from splinting

is an accumulation of air between the parietal and the visceral pleura.

• –Physical findings include hyperesonance 
• with chest percussion, decreased or absent breath sounds, and lung collapse on chest film.

• –Nitrous oxide is contraindicated in these
• patients.

• –Treatment consists of placing a chest
• tube in the fourth of fifth intercostals space anterior to the midaxillary line. (a persistent leak after tube placement may indicate injury to a major bronchus.) Air is forced into the thorax with inspiration and cannot escape during expiration.

• ; Ipsilateral lung collapses and trachea and
• mediastinum are shifted to the contralateral side.

• –A simple pneumothorax can develop into a
• tension pneumo with positive pressure ventilation.

–Venous return and expansion of contralateral lung are impaired.

–Clinical signs include ipsilateral absence of breath sounds, tracheal and mediastinal shift, hyperresonance with percussion, and distended neck veins.

A flail chest occurs when a segment of the thoracic cage is separated from the rest of the chest wall.

• –This is usually defined as at least two
• fractures per rib (producing a free segment), in at least two ribs.

• –A segment of the chest wall that is flail
• is unable to contribute to lung expansion. (Chest wall can’t participate in ventilation.)

• - Pulmonary contusion is an injury to
• lung parenchyma, leading to edema and blood collecting in alveolar spaces and
• loss of normal lung structure & function. 
• (results in worsening respiratory failure over time. )

• –This blunt lung injury develops over the
• course of 24 hours, leading to poor gas exchange, increased pulmonary vascular
• resistance and decreased lung compliance.

• –There is also a significant inflammatory
• reaction to blood components in the lung, and 50-60% of patients with significant pulmonary contusions will develop bilateral Acute Respiratory Distress Syndrome (ARDS).

–Pulmonary contusions occur in approximately 20% of patients with severe blunt trauma and it is the most common chest injury in children.

-Haemothorax is a collection of blood in the pleural space and may be caused by blunt or penetrating trauma.

–Most haemothoraces are the result of rib fractures, lung parenchymal and minor venous injuries, and as such are self-limiting.

–Less commonly there is an arterial injury, which is more likely to require surgical repair.

–Most small-moderate haemothoraces are not detectable by physical examination and will be identified only on Chest X-ray, FAST,or CT scan.

–Large hemothoraces that are clinically detectable must be treated promptly.

• –Massive hemoptysis may require isolation
• of the affected lung with DLT or endobronchial blocker tube. (This will also allow for ventilation of unaffected side.)

–If separation is not possible or even moderate airway pressures will cause considerable bronchial leaking, jet ventilation is used.

•   (air leakage from traumatized bronchi can track an open pulmonary vein causing
• pulmonary and systemic air embolism. Need to fix the leak!

May indicate the presence of a pneumothorax or laryngeal, tracheobronchial, or esophageal trauma.

–Pneumothorax and hemothorax may lead to respiratory and cardiovascular collapse.

• –Requires immediate chest tube before
• induction of general anesthesia.

• – Avoid central line insertion on the side
• opposite of an injury because of the potential consequence of bilateral pneumothorax.  Avoid ipsilateral side if a concomitant major venous injury is suspected.

• Physical findings of a simple
• pneumothorax

N2O contraindicated

• CT
• in 4th IC space

• Simple
• pneumo can become a tension pneumo with PP ventilation

• delayed pulmonary complication of trauma
• caused by:  sepsis, direct injury, aspiration, head injury, fat embolism, massive transfusion, and oxygen toxicity (secondary injury).

–Mortality of ARDS approaches 50%.

–Most anesthesia ventilators are not equipped to handle the ARDS patient (ICU ventilators).

1.  General anesthesia almost always required.

• 2.  Patients may need prolonged ventilatory
• management postoperatively.

3.  Nitrous oxide has no place in chest trauma.

4.  Monitor airway pressure vigilantly.

• 5.  Plan for lung isolation and one lung
• ventilation if bleeding is intractable. DLT may prevent blood from flooding unaffected side and may be a life saving measure.

• 6.  Regional anesthesia (as an adjunct i.e.,
• intercostal nerve blockade or thoracic epidural anesthesia) may be useful for analgesia with multiple rib fractures.

• 7.  Adequate analgesia can reduce chest wall
• splinting, regional hypoventilation, and progressive hypoxemia.

Blunt cardiac trauma—results in muscle contusion, chamber rupture, or valvular disruption

• usually diagnosed by ECG changes (STs),
• cardiac enzyme elevations, or abnormal echo.

•Can have severe wall motion abnormalities.

•High risk for arrhythmias, such as heart block,and V-fib.  Elective surgery is postponed until all heart injury resolve.

• •Great vessel injury consists of aortic
• dissection and transection; avulsion of the subclavian artery, aortic or mitral valve
• disruption, diaphragmatic herniation, and esophageal rupture.

associated with injury to sternum, hemothorax, pericardial tamponade, myocardial tamponade, myocardial dysfunction, valvular dysfunction and ECG changes (sinus tach,PVCs, bundle branch block, ST segment changes, and overt ischemia.)

• 1. distended neck veins,
• 2. muffled heart sounds,
• 3. hypotension-present in only 30% of patients with pericardial tamponade/ pulsus paradoxis is even less accurate.

•Choice diagnostic is cardiac ultrasound.

•Pericardiocentesis may be used to stabilize patient until surgical repair is performed.

•Surgical treatment is thoracotomy.

•Subclavian artery—Subject to injury with hyperextension of neck and shoulder.

The structures at risk in penetrating neck injury are primarily the airway, vascular structures, the esophagus, spinal column including the spinal cord, the lower cranial nerves and the brachial plexus. The thoracic duct is also at risk in wounds of the left neck.

• •following blunt trauma and hemorrhagic
• shock has a dismal prognosis.  (Low
• perfusion arrest) (severe ischemic myocardial damage and ischemic damage to
• other organ systems).

• •Manifests as severe arterial hypotension,
• electromechanical dissociation, ventricular standstill.

•Profound hyopothermia usually leads to cardiac demise and may be the result of massive cellular necrosis as well as the cause of cardiac arrest.

•Maximize inotropy, heart rate, and preload. 

• •Penetrating injury to heart or great
• vessels requires immediate surgical repair.

• •Repeated manipulation of heart results in
• frequent hypotension and bradycardia intraoperatively.

• •Ruling out traumatic aortic rupture by
• emergency angiography after noted widened mediastinum. (test of choice is angiography and TEE ).

•Often severely hypovolemic.

• •May require cardiopulmonary bypass for
• certain repairs

•Have crossmatched blood on hand or O negative blood Prior to induction.

• •Inotropic agents and vasopressor agents
• should be immediately available.

• •Rapid fluid infusers (level 1) set up and
• ready.

Causes; penetrating injury, paralytic ileus, peritoneal irritation (muscle guarding, percussion tenderness

• •Most frequently injured abdominal organ
• in blunt trauma.

• •Symptoms; abdominal or referred shoulder
• pain, abdominal rigidity, falling Hct, or hypotension.

•Many are managed non-surgically.

• •Active bleeding spleen or avulsed spleen
• requires splenectomy.

•frequently injured in blunt trauma

•Noncomplex injuries are managed non-operatively.

• •Operative management –laparotomy for
• complex, severe injuries with large blood loss and high mortality.

•Large amounts of unclotted blood may present in the abdomen (hepatic or splenic injury) with minimal signs. (surgeon will often explore abdomen for bleeding first)

•Diagnose with free air on abdominal radiograph ( or bloody aspirate from peritoneal levage)

• •Opening of abdomen may be followed
• by severe hypotension as tamponade effect is lost.

• Rapid fluid infuser prior to surgically
• opening the abdomen.

•Avoid nitrous oxide.

• •Nasogastric tube ( when should this be
• placed orally?)

• •Massive blood loss from major vascular,
• hepatic, splenic, renal, pelvic fractures, retroperitoneal damage) 

•Potential for massive blood transfusion.

• •Transfusion-induced hyperkalemia is
• equally as lethal as exsanguinations and must be treated aggressively.

• • Aorta may need to be clamped to repair
• injured vessels. (Clamp times and ischemic injury).  Assess for rhabdomyolysis and acute renal failure.

• • Bowel edema from fluid , tight closures
• can cause abdominal compartment syndrome causing renal and splanchnic ischemia,
• compromised ventilation, and renal perfusion.

• Abdomen often left open.

• •All multiple trauma patients have a Foley
• catheter. (assess bleeding into renal pelvis or bladder).

•Pelvic or perineal injury evidence by; blood at the urethral meatus, a perineal hematoma, or a high riding prostate.

•Patient may require retrograde urethrography before catheterization.

• •Radiographic kidney-ureter-bladder for
• penetrating abdominal and back injuries and undergo IV pyelography or contrast
• enhanced CT scan.

• •Most renal injuries (85%) can be managed
• non-operatively.

• •Refractory hypotension necessitates
• immediate surgical intervention.

•Injury to the urethra can result in a patient’s inability to urinate or clinical signs of direct injury .

•Diagnostic urethrography should precede suprapubic cystostomy for urinary drainage and control of hemorrhage.

•Check peripheral pulses in all extremities during evaluation. (all trauma patients).

• Arteriography to define injuries.

• •Anesthetic management should focus on
• controlling hemorrhage and operative repair of effected vessels.

• •Regional anesthesia should be considered
• in stable patients.

•4-6 hours of limb ischemia can cause irreversible tissue necrosis.

Orthopedic trauma often exists with peripheral vascular damage

• •Assess for damage to sympathetic chain
• (Horner’s syndrome)( what might you see)

• •Medial clavicle fracture dislocating
• clavicle upward and retrosternally ( Airway, tracheal injury) (shoulder gets hit from the side)

•Dislocation of glenhumoral joint can cause axillary nerve injury. 

Shoulder—hyperabduction, depression of the shoulder girdle, brachial plexus tear.

Associated with radial nerve injury (especially the middle or distal part)

• Peripheral ischemia and compartment
• syndrome from edema risks nerve and muscle necrosis.  May require fasciotomy.

• Median nerve compression. May require
• division of transverse carpal ligament.

1. Exsanguinating hemorrhage—external bleeding in open fractures or from retroperitoneal hematoma in closed fractures (0.5% to 1.0%). Almost always present with either severe hypotension or cardiac arrest and rarely respond to resuscitative measures.

• 2. Hemodynamically stable—uncomplicated
• course (75%) Urgent or elective repair of bony disruptions

• 3. Intermediate group--  Critical condition with various degrees of overall injury and
• hemodynamic stability (25%).

•Initial mangement

• •External pelvic fixation, compression
• binder for “open book fracture”, Pelvic angiography

• •Bed rest and ORIF for type I Anterior
• Posterior Compression (APC) injury or lateral compression type I.

• •APC II – widened sacroiliac joint with
• hemorrhagic vascular consequences require acute external fixation with delayed
• conversion to internal fixation, acute ORIF, or arterial embolization.

can occur with pelvic or major ling bone fractures.

    May cause pulmonary insufficiency, dysrhythmias, skin petechiae, and mental deterioration with 1-3 days after the traumatic event.

•may be associated with myoglobinuria. 

Early reversal of hypovolemia and alkalinazation of the urine may help prevent acute renal failure

• •most common major skeletal injuries; can
• be associated with neurovascular trauma.

• •-can be associated with 3 units of occult
• blood loss.

•common in the elderly  ( on top of many existing medical illnesses)

• –Traction initially for pain relief,
• require ORIF to ensure adequate healing and function.  Avoid prolonged immobilization.

• –Regional and combined techniques can be
• considered for stable patients with isolated injuries.

• –Stable patients with digit or upper
• extremity amputation without crush injury or tearing of vessels and nerves.

• –Lengthy procedures, in some cases greater
• than 24 hours.

• •General anesthesia often chosen due to
• the length of case and the need to control hemodynamics.

• •Combined techniques preferred when
• possible for optimal post-op pain control and improvement of blood flow with sympathectomy.

•Avoid pressure injuries intra-op (especially head and scalp) and check endotracheal cuff pressure periodically if nitrous oxide is used.  (lengthy cases)

•Warm the patients and well hydrated.  Avoid hyperventilation or the use of vasoconstrictors. (why?)

•Consider invasive monitoring for optimization of perfusion pressure and due to length of case or rotate NBP cuff.

•Determine need for anticoagulation intraoperatively.

•Don’t let blood loss get ahead of you.  Send periodic hgb/ABG and closely watch for signs of hypovolemia (what signs?).

•Rule of nines --Adults:  The head and each upper extremity represents 9% total body surface area. The anterior trunk, posterior truck, and each lower extremity represent 18%

•Depth of burn determines therapy.

•Partial thickness vs. full thickness burn

• •First degree burns—limited to the
• epithelium, painful, red and blanches to touch (partial thickness burn)

• •Second degree burn—Extend into the
• dermis, painful, (partial thickness burn).

• •Third degree burn—full thickness,
• insensate, destroys nerve endings.

•Impairs skin’s ability to regulate temperature, fluid and electrolyte balance, provide a barrier to pathogens.

•Massive fluid shifts, protein loss, heat loss, and infection commonly occur.

•Major burns- systemic inflammation, hypermetabolism, and immune suppression occur as a result of circulating mediators.

• •Cells become more permeable to sodium-
• generalized swelling (vasoactive substances are released from burned tissue)(edema occurs in both burned and unburned tissue)

• 1. Microvascular permeability—significant
• tissue edema 12-24 hours after thermal injury.

• •Water, electrolytes, protein lost in
• large amounts into extravascular space.

•Intravascular hypovolemia results—hypovolemic shock (burn shock).

2. Initial decrease in cardiac output due to reduced responsiveness to catecholamines and circulating humoral factors.

• •SVR increased (coinciding with decreased
• CO)

• •Magnitude of changes depends on extent of
• injury

• 3. Increase in cardiac output 24 –48 hours
• after burn injury (successful resuscitation)

Reduced SVR- consistent with pathophysiology of systemic inflammatory response syndrome.

•Hypermetabolic state exists 3-5 days after injury.

• •Caloric requirements are 1.5 to 1.7 times
• normal after major thermal injury (protein requirement 2.5g/kg/day).

• •Goal is to reduce muscle catabolism and
• bacterial translocation through intestinal mucosa

•Keep normothermic ( do not strain metabolic requirements)

•Hemoconcentration—from capillary leakage immediately after injury.

• •HCT can remain increased after 48 hours
• despite fluid large IV fluid intake.

• •Bleeding and a shortened erythrocyte
• half-life can result in anemia.

•Thrombocytopenia—results from micoraggregation of platelets in the skin, smoke damaged lung tissue and aggressive volume resuscitation.  (occurs early after injury)

•DIC- thrombotic and fibrinolytic mechanisms are activated in major burn injuries.

•Antithrombin III, protein C, and S, increase the thrombogenicity of burn patients later in their clinical course—risk of DVT and PE.

associated with high mortality

•Decreased renal blood flow due to hypovolemia and decreased CO, increased catecholamines, aldosterone, and vasopressin, can lead to renal failure.

• •Other mechanisms include nephrotoxic drug
• effects, rhabdomyolysis, hemolysis, and sepsis.

• •Intestinal ileus diminishes GI function
• immediately after burn major burn injury.

• •Nasogastric tube to vent stomach and
• prevent aspiration.

• •Curling’s ulcers (mucosal erosion)—More common in children.  May lead to gastric
• perforation.  Treated with H2 antagonists
• and antacids.

Gastrointestinal complications—esophagitis, tracheoesophageal fistula (from prolonged intubation and nasogastric tube), hepatic dysfunction, pancreatitis, acalculous cholecystitis, and mesenteric artery thrombosis.

•Infection--  Bacterial infiltration of underlying tissue may cause septicemia.  Common organisms involved are staphylococci, beta-hemolytic streptococci, and Gram negative rods such as Pseudomonas and Klebsiella

• •Treated with topical antimicrobials and
• early skin grafting.

Muscle acetylcholine receptors—Proliferate at the burn site and at sites distant from the burn injury. 

–Increase resistance to non-depolarizers.

–Prolonged block with depolarizers.  May be safe for the first 24 hours.

• –May cause life threatening hyperkalemia
• during later stages.

Initial evaluation of the burn patient:

• •Airway and breathing--- Massive edema of
• epiglottis or larynx to either dry air at 300 C or 100 C steam.  Leads to rapid airway obstruction.

• •Chemical products can dissolve in the
• tracheobronchial tree forming acids that irritate the mucous membranes of the
• respiratory tract.

• •Airway soft tissues can become quickly
• distorted making intubation difficult or impossible.

• •Circumferential full thickness burns of
• the thorax will decrease chest wall compliance 
• and lead to hypoxemia and respiratory failure.  May require escharotomies.

•Smoke inhalation injury—Suspect inhaltion injury when there are burns to the head and neck, singed nasal hairs; swelling of the mucosa of the nose, mouth, lips, or throat, or black charry clored sputum.

• •Both upper airway and parenchyma may be
• affected.

• •Chemical products of combustion combine
• with water in the respiratory tract to form strong acids and alkali, causing bronchospasm, edema, and mucous membrane ulceration. 

• •Inhalation of gases such as phosgene and
• sulfuric acid can damage alveolar membrane and cause partial or complete airway
• obstruction.

• •Combustion of polyurethane-containing
• products releases hydrogen cyanide, which causes tissue asphyxia by inhibiting
• cytochrome-oxidase activity.

• •May cause an anion gap metabolic acidosis
• and an elevated mixed venous PO2.  Plasma
• lactate levels correlate with cyanide levels.

• •Treatment is supportive but can include
• administration of sodium nitrite (300 mg IV over more that 5 minutes in a volume of 100ml of 5% dextrose) and sodium thiosulfate (12.5 g) and, in severe
• cases, inhaled amyl nitrate.

• •Indirect lung injury—Not from
• inhalational burn but from circulating wound mediators, decreased wound oncotic
• pressure, and complications of burn therapy.

• •Carbon monoxide—binds to hemoglobin
• displacing oxygen; left shift of oxyhemoglobin curve.

•Tissue hypoxia-100% oxygen

• •Oxyhemoglobin and carboxyhemoglobin absorb infrared light at the same
• wavelength.  O2 sat inaccurate. Diagnosis
• made on clinical suspicion, and measurements of carboxyhemoglobin measured with a spectrophotometric CO monitor.

•Half life of CO is inversely related to FIO2.  ( 5-6 hours on RA, 30-60 mins on 100% O2)

•Hyperbaric oxygen in severe cases.  Supportive care with 100% O2 generally.

•Fluid replacement mainly with crystalloid.

• •Standard protocols based on body weight
• and amount of surface area burned (TBSA)

• 1. Parkland formula—Used at Mass General.  4.0 mL of Ringer’s lactate per kg per % TBSA
• burned per 24 hours.

2. Brooke formula: 1.5 ml of crystalloid per kg per % TBSA burn per 24 hrs plus 2,000 mL of 5% Dextrose in water per 24 hours.

• •Half the calculated fluid deficit is
• administered during the first 8 hours post-burn and the remainder is administered over the next 16 hours.  The patient’s daily maintenance fluid requirements are given concurrently.

• •The endpoints of fluid therapy are
• hemodynamic stability and maintenance of an adequate urine output.  In extensive burns, fluid management is adjusted according to appropriate invasive monitors and laboratory studies.

•ABCs since burns are a form of trauma

• •Obtain a history of preexisting diseases,
• age, and extent of present burn injury.

• •Assess for likely pharmacokinetic
• alterations, drug tolerance, difficult IV access, and airway access difficulties due to anatomical airway derangements.

•Airway—Early edema may make masking and laryngoscopy difficult.

•IV access and monitoring

•Large bore Ivs are mandatory

• •ECG electrodes may be placed directly on
• debrided tissue. Needle electrodes may be used if available.

•Arterial lines—Indispensable for monitoring and sample access.  May need to be placed through burn injury if no unburned site available.

• •CVP—central access and central pressure
• monitoring.

• •Pulmonary artery catheter—May be
• necessary for patients with myocardial dysfunction, sepsis, or persistent
• oliguria or hypotension.

• •Muscle
• relaxants:

• a. Succinylcholine safe in the immediate
• hours after burn injury.  Dangerous after
• the first 12-24 hours after injury and may produce profound hyperkalemia and
• cardiac arrest.

• b. Non depolarizers- may show a
• diminished response.  May in some cases
• require 3 to 5 times the dose.

•Anesthetic agents--No single preferred agent.

• •Ketamine and etomidate may have advantages in patients with
• uncertain volume status.

• •My have greatly increased opioid
• requirements due to tolerance and an increased volume of distribution.  Doses may be massive.

•Temperature regulation

• •Most comfortable temperature is about 100
• degrees (38 C)

• •Maintain normotemperature. 
• Warm humidified rooms. All fluids and blood products should be warmed.  All inspired gases should be warmed. 

• •Place pediatric patients under a radiant
• heat source and warming blanket whenever possible.

Immunosuppression

• •Immune system is suppressed for weeks to
• months.

• Every effort should be made to practice
• aseptic technique with line insertion, airway suctioning, and handling of patient

Post-anesthetic care

•Maintain normothermia—shivering leads to vasoconstriction and may impair graft perfusion.  Supplemental oxygen given until fully recovered.

• •Titrate analgesics for adequate pain
• control.

•Begins at the macrocirculatory level and is mediated by the neuroendocrine system.

• •Decreased BP leads to vasoconstriction
• and catecholamine release.

• •Blood is shunted to preserve heart and
• brain and major organs.

• •Pain, hemorrhage, and cortical perception
• of traumatic injuries lead to the release of a number of hormones—renin-angiotensin, vasopressin, ADH, growth hormone, aldosterone, glucagons, cortisol, epinephrine, and norepinephrine.

• •Ischemic cells respond to hemorrhage by
• taking up interstitial fluid—depleting intravascular fluid.  This creates a “no reflow” situation in the adjacent capillaries and microcirculation.  (This creates a non reversible ischemic situation even in the presence of adequate macrocirculation.)

• •Ischemic cells produce lactate and free
• radicals causing direct cellular damage and from the bulk of the toxic load that will be washed back into central circulation when flow is reestablished.

•Inflammatroy mediators are also releases such as, prostacyclin, thromboxane, prostaglandins, leukotrienes, endothelin, complement, interleukins, tumor necrosis factor and others.

• •Once mediators are released, organ system
• ischemia and failure can occur even when adequate perfusion (macro) is achieved. Patients can die of multi-organ system failure (MSOF) even when bleeding has been controlled.

• •The CNS is the prime trigger of the
• neuroendocrine response to shock, which maintains perfusion to the heart, kidney, and brain at the expense of other tissues.

• •Brain activity is decreased during shock
• and hypotension (reflex and cortical) they are reversible with adequate resuscitation but may be permanent with prolonged ischemia.

• •Failure to recover pre-injury neurologic
• function is a marker for poor prognosis.

• •Produce renin, angiotensin, aldosterone,
• cortisol, erythropoietin, catecholamines.

• •Kidney manages glomerular filtration
• during hypotension by selective vasoconstriction of  and concentration of blood flow in the medulla and deep cortical area.

• •Tubular necrosis, cell death, and renal
• failure occur when kidneys are unable to concentrate blood flow.

• •Relatively preserved from ischemia by
• maintaining or increase cardiac blood flow until late stages.

• •Lactate, free radicals act as negative
• inotropes and may produce cardiac failure in a decompensated patient.

•Patients with cardiac disease have a fixed ventricular stroke volume and are unable to increase cardiac output in states of shock and are therefore susceptible to cardiac collapse, as are those with direct cardiac trauma.

• •Tachycardia is the only option and may
• worsen ischemic condition.

•Elderly patients are particular susceptible to cardiac failure and may not respond favorably to fluid resuscitation.

• •The lungs is the destination for the
• inflammatory by products of an ischemic body.

• •Immune complexes and cellular factors in
• pulmonary capillaries leads to neutrophil and platelet aggregation, increased permeability, destruction of lung architecture, and ARDS.

• •Sentinel organ in MOSF in traumatic
• shock.

• •Pure hemorrhage in the absence of hypoperfusion does not produce pulmonary
• dysfunction.  This evidence that traumatic shock is more than just a hemodynamic disorder.

•One of the earliest organs affected by hypoperfusion and may be the  trigger for MOSF.

• •Early vasoconstriction and “No reflow”
• phenomena. 

• •Increased bacterial translocation to the
• liver and lung after ischemic death to intestinal wall.

• •Liver is said to suffer from reperfusion
• injury after recovery from shock. 
• Hepatic cells are metabolically active and contribute to the ischemic inflammatory response and to irregularities in blood glucose.

• •Skeletal muscle tolerates ischemia better
• than other organs because cells are not as metabolically active.  Because of it’s mass, produces a large amount of lactate and free radicals from ischemic cells.

• •Sustained ischemia of muscle cells leads
• to an increase in intracellular sodium and free water with an aggravated depletion of fluid in the vascular and interstitial compartments.

•Fluid is lost because of blood loss,uptake by ischemic cells, and extravasation into the interstitial space.

• •Fluid therapy Increases cardiac output
• and blood pressure in a hypovolemic patient.

• •May also cause hypothermia, dilution of
• red cell mass decreasing oxygen delivery, and coagulopathy.

• •The result of aggressive fluid
• administration can cause a transient increase in blood pressure followed by
• increased bleeding and more hypotension necessitating more fluid infusion.

• •Fluid therapy for hypoperfusion has been a source of controversy for
• decades.

• •Resuscitation must be looked at in two
• phases.

• •Early-- While patient is still actively
• hemorrhaging.  Much more complex and
• risks of causing ongoing hypoperfusion are greater.

• Late-- Once hemorrhage has been
• controlled.  Driven by target goals and
• maintain adequate oxygen delivery.

Types of Resuscitation fluids:

•Isotonic crystalloids-NS, Ringer’s lactate, Plasma Lyte A.  Initial crystalloid infused to trauma patients.

• •Advantages: Inexpensive, readily available,
• non-allergenic, noninfectious.  Easy to
• warm, effective in restoring total body fluid volume, easily infused with most
• medications.

•Disadvantages: No oxygen carrying capacity, lack of coagulation ability, and limited intravascular half-life. 

• •Some have recently been implicated as
• being immunosuppressive and triggers for cellular apoptosis.  (in rat models LR was seen to increase apoptosis in the liver after resuscitation and as a reperfusion injury Where whole blood and hypertonic saline did not).

• •Hypertonic saline—(with or without Dextran)  In theory, HS will draw interstitial fluid
• into the intravascular space and reverse some of the non-hemorrhagic fluid
• losses cause by shock and ischemia.

• •Animal studies have shown HS to be
• efficacious in improving survival following large blood loss trauma but
• evidence on human trauma patients has been inconclusive.

• •HS is commonly used as an osmotic agent
• in the management of TBI with increased ICP.

• •Colloids—Hetastarch solutions, albumin.  Fluid volume expanders. Readily available,
• easily stored and administered, relatively inexpensive.  Like HS, they work to draw fluid into the
• intravascular space. 

• •When IV access is limited, colloidal
• resuscitation will restore intravascular volume more rapidly than crystalloid
• infusion will and at a lower volume of administered fluid.

• •They have no oxygen carrying capacity and
• their dilutional effect on blood will mimic that of
• crystalloids.

• •Studies have demonstrated no great
• benefit of colloids over crystalloids  in
• a variety of resuscitation models.

• •The dilution of circulating blood volume
• by colloid and crystalloid infusions have led to an increase of blood products in the management of early hemorrhagic
• shock. 

•Improve oxygen carrying capacity.  Avoid dilutional coagulopathy by the early use of FFP.

•Unit of blood has a HCT of  60% – 70%.

• •Restores oxygen delivery and expands
• intra-vascular volume. May produce a lethal transfusion reaction.  Carry dozens of minor antigens which may produce a reaction in susceptible patients. 
• Risks of transmitting infectious agents and hypothermia. 

• •May lower a patient’s temperature rapidly
• if not on a warming device. 

• •Premixing with NS will decrease viscosity
• and allow for more rapid infusion.

• •Risk of infectious transmission of any
• agent is 1:63,000; Hep C 1:150,000; HIV 1:1,000,000.

• •Major transfusion reaction 1:100,000 for
• cross-matched blood.

• •Cross-matched blood takes about an hour
• to get to the patient from the time the sample reaches the blood bank.

• •Type specific blood takes about one half
• hour.

• •Citrate intoxication. 
• Citrate is an anticoagulation agent in packed cells and binds free
• calcium (clotting factor IV)  Multiple
• consecutive units of transfused blood units overwhelms the body’s ability to
• mobilize free calcium and cause a marked reduction in circulating free calcium
• with a profound negative inotropic effect on the heart. 

• •Unrecognized hypocalcemia is a common cause of hypotension that
• persists despite an adequate volume of resuscitation.

• Ionized calcium levels should be
• monitored at regular intervals in a hemorrhagic patient,and calcium should be administered as needed

•Hemoglobin-based oxygen carriers (HBOCs).--  long shelf life, lower cost, no need for cross-matching, and minimal risk of viral transmission. 

• •Concerns over potential for inappropriate
• vasoconstriction and hypertension as a result of increased scavenging of NO and
• potentiation of coagulopathy because of platelet impairment.  The only human trail using HBOCs in trauma did not produce these findings, but also did not produce evidence of survival
• benefit.

• •At smaller doses, HBOCs may facilitate
• delivery of oxygen to ischemic tissues.

• • A four year retrospective cohort study of
• critically injured patients requiring emergency surgery revealed 140 patients
• who received 20 units or more of packed red blood cells.

• •The determining factor on their survival
• had less to do with the amount of blood lost and the amount of blood
• transfusion they received, but more on the depth and duration of their shock
• state.

• •The number of blood units did not differ
• between the survivors (30%) and the non-survivors (70%). 

• •Eleven variables were found to be
• significant in these patients: the use of an aortic clamp for control of BP,
• use of inotropic drugs, time with systolic BP less than 90 mmHg, time in the
• OR, temp lower than 34 degrees, urine output, pH less than 7.0, PaO2/ FIO2
• ratio less than 150, PaCO2 higher than 50 mm Hg, potassium greater than 6mM/L,
• and calcium less than 2mM/L.  Presence of
• the first three in the patients studied were invariably fatal.

• •Plasma—indicated for the treatment of
• coagulopathy from resuscitation of hemorrhagic shock.  Volume expander.  Risk of infectious transmission is same as
• PRBCs.  Must also be warmed, especially
• in early resuscitation. 

• •Not usually necessary for transfusions of
• 1-4 units of packed cells due to sufficient coagulation factor reserves. 

• •Massive blood loss of up to one blood
• volume or 10 units of packed cells will generally require one unit of plasma
• for each unit of PRBCs.  (need for plasma
• with loss of 5-9uints is variable.)

• •Coagulation parameters (prothrombin time, INR, partial thromboplastin time, fibrinogen) should be measured
• frequently during resuscitation. 

• •Hemorrhage exacerbates coagulopathy
• begetting further hemorrhage.

• •Plasma and PRBCs should be administered
• on a 1:1 ratio to any patient with obvious massive hemorrhage, even before lab
• studies are available.

• •Plasma requires blood typing but not
• cross-matching.

•Needs to be thawed.  Request early in anticipation of use.

• •Platelet—transfusions of platelets should be
• reserved for patients with clinically coagulopathy and low pLT count <50,000 cells/mm3.

• •Although the development of coagulopathy
• in elective surgical patients is usually the result of platelet deficiency, the same is not true in trauma patients, who are more apt to suffer from consumption of coagulation factors.

• •Transfused platelets have a very short
• half-life and should be reserved only to patients with visible
• coagulopathy. 

• •Platelets should not be transfused
• through filter, warmers, or rapid infusion devices because they will bond to
• the inner surfaces of these devices and reduce the quantity of platelets
• actually reaching the circulation.

IV Access

•Place at least two 16 g or larger IV catheters.  IJ requires the collar to come off and manipulate the neck.  Femoral vein access may contribute to bleeding if trauma to the inferior vena cava or penetrating abdominal trauma.

•FV cannulation also carries a high risk of DVT. Femoral lines should be removed as soon as the patient stabilizes. 

•Subclavian approach is beneficial because this area is seldom directly traumatized and easily visualized.

•High risk for pneumo. If pt. Has a chest tube, place SC line on same side if possible.

• •Arterial lines are important but their
• placement should not supercede other therapeutic or diagnostic interventions.

•Hypothermia may have a place in acute trauma, but for now, we know that hypothermia will:

–potentiate dilutional coagulopathy, systemic acidosis, and shivering and vasoconstriction, increased metabolic demand and possibly myocardial ischemia.

•All IV fluid should be warmed.  All warming interventions should be maximized early.

• •Warm room, cover your patients, bair huggers. Make sure they have these
• interventions when they go to radiology, ED, and PACU, Angiography, not just
• the OR. 

• Rapid fluid infusers—

• –Benefit-- rapid warming of patient, rapid
• replacement of intravascular volume, reduction of acidosis.

• –Risk—Over-infusion of IV fluids, elevated
• BP, may contribute to re-bleeding.

• •Try to keep basal fluid administration
• low (200 to 500 mL/hr) with small fluid boluses to control systolic BP 80 to 90 mmHg before control of hemorrhage.

Late Resuscitation:

• •The adequacy of resuscitation should not
• be based on the presence of normal vital signs, but by normalization of organ
• and tissue perfusion. 

•Appropriate fluid, Appropriate amount, and Appropriate time.

• •Late resuscitation begins once the
• bleeding is definitely controlled by surgery or the presence of time.

• •Goal is to restore normal perfusion to
• all organ systems while continuing to support all vital functions.

•Hypoperfusion from shock continues to produce biochemical derangements long after bleeding has been corrected.

• •THE DEPTH AND DURATION OF SHOCK IS
• HIGHLY CORREALTED WITH THE EXTENT OF SUBSEQUENT ORGAN FAILURE.

• •Traditional vital sign markers, such as
• BP, HR, and urine output have been shown to be insensitive to the adequacy of
• resuscitation.

• •There is current evidence to support that
• the adequacy of left ventricular performance post-resuscitation is correlated with improved lactate clearance and improved survivability.

•Occult hypoperfusion syndrome is common in postoperative trauma patients, particularly young ones. This syndrome is characterized by normal BP maintained by intense systemic vasoconstriction—

• •Intravascular volume is low, CO is low,
• and organ ischemia persists.  Such patients are at high risk for MOSF if hypoperfusion is not promptly corrected.