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Table 32.3 Common genetic syndromes associated with pheochromocytomas or paragangliomas
Pheochromocytoma or
Syndrome Gene Location Multiple endocrine neoplasia, type 2A
(MEN 2A) Multiple endocrine neoplasia, type 2B
(MEN 2B)
Von Hippel-Lindau disease (VHL) VHL 3p26-25 Pheochromocytoma Renal cell carcinoma
Neurofi bromatosis type 1 disease (NF1) NF1 17q11.2 Pheochromocytoma Neurofi bromatosis
Familial paraganglioma 1 SDHD 11q23 Both Familial paraganglioma 4 SDHB 1p36.1–35 Both
Adapted from Elder et al. [
1 ]
RET 10q11.2 Pheochromocytoma Medullary thyroid carcinoma
RET 10q11.2 Pheochromocytoma Medullary thyroid carcinoma
paraganglioma Associated symptoms or diagnoses
Primary hyperparathyroidism
Ganglioneuroma Marfanoid habitus
Hemangioblastoma Pancreatic islet cell tumors
Café au lait spots Axillary or inguinal freckling Optic nerve glioma
L.E. Kuo and D.L. Fraker
which have other manifestations (see Table 32.3 ). However, familial pheochromocytomas may also exist outside of these well-defi ned syndromes [ 106 ]. These syndromes may affect the PCC patient, necessitating further treatment, or may affect a family member. Genetic testing should only be per­formed on PCC patients at high risk for a genetic mutation to better inform treatment decisions; “high risk” is defi ned as patients with a family history of pheochromocytoma or another genetic syndrome component, patients with multifo­cal, metastatic or extra-adrenal disease, or patients younger than 50 years of age [ 1 , 106 ].
There is no evidence on the optimal timing of genetic test­ing: some syndromes are associated with multifocal or bilat­eral pheochromocytomas, which all may contribute to the episode of PCC. Genetic testing prior to surgical intervention may therefore be helpful in guiding surgical management. However, genetic testing in a timely fashion may not be fea­sible in all situations, and delaying surgery due to genetic testing may not be possible or may provide an opportunity for further crisis episodes. PCC in a patient with a genetic syndrome has not been described in the literature, and there is no evidence or expert opinion to guide the timing.
Conclusion
Pheochromocytoma crisis is a rare event but should be
considered in critically ill patients presenting with multiple
organ system failure. Timely diagnosis and individualized
management are essential to patient survival.

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Trauma

D. Joshua Mancini , Mark J. Seamon , and C. William Schwab
3 3

General Approach

The care of the trauma patient in the intensive care unit (ICU) follows the same principles as the care of the patient in the trauma bay. An initial focus on airway, breathing, circula­tion, and disability allows for an expedited initial assessment of the trauma patient that arrives in the intensive care unit. All of the adjuncts available to the staff in the trauma bay should also be available in the ICU, from point of care test­ing to ultrasound. Once life-threatening issues have been addressed, an organ system approach to the patient can be implemented. Radiologic studies and reports as well as labo­ratory values obtained in the trauma bay must be reviewed.
Critically injured patients typically progress through four phases: the resuscitative phase, the early life-support phase, the prolonged life-support phase, and the recovery phase [ These can be grouped into early and late stages of ICU care. The early stage includes the resuscitative phase and early life support. The resuscitative phase is a continuation of trauma bay or operating room resuscitations and encompasses the fi rst 24 h. Management during this phase, which often involves several concurrent treatment and diagnostic maneu­vers, is focused on control of active hemorrhage, aggressive resuscitation, and restoration of tissue oxygenation. By 24–72 h, diagnosis of occult injuries is complete, and
1 ].
treatment aims are focused on specifi c organ failures during the early life-support phase. Early multiple organ dysfunc­tion syndrome, commonly involving pulmonary, cardiovas­cular, and renal failure, may become apparent at this time.
After 72 h, clinical priorities shift. This later stage of ICU care includes the prolonged life-support and recovery phases. The prolonged life-support phase focuses on support of the patient with nutrition, ventilator liberation, continuation of prophylaxis regimens, and attempts to prevent secondary complications that could impair the recovery of the patient. Meticulous and vigilant ICU care is necessary during this time for prevention and early detection of complications. The duration of this prolonged life-support phase is highly variable and depends largely on injury severity and associ­ated complications. The recovery phase is marked by the transition from ventilatory support to spontaneous breathing and removal of invasive monitoring devices. Rehabilitation with physical and occupational therapy, begun during the life-support phase, is continued and intensifi ed. Both the patient and the family are prepared for the transition from the ICU to general patient or intermediate care unit, and plans for further convalescence and rehabilitation are developed.

Initial Assessment

Life-threatening issues may have been addressed in the
D. J. Mancini , MD (*) Department of Surgery , Dartmouth-Hitchcock , Lebanon , NH 03756 , USA
david.j.mancini@hitchcock.org
e-mail: M. J. Seamon , MD
Division of Traumatology, Surgical Critical Care & Emergency Medicine , Hospital of the University of Pennsylvania , Philadelphia , PA 19104 , USA
mark.seamon@uphs.upenn.edu
e-mail: C. W. Schwab , MD, FACS
Department of Surgery , Hospital of the University of Pennsylvania , Philadelphia , PA 19104 , USA
moorek@uphs.upenn.edu
e-mail:
© Springer International Publishing Switzerland 2016 N.D. Martin, L.J. Kaplan (eds.), Principles of Adult Surgical Critical Care, DOI 10.1007/978-3-319-33341-0_33
trauma bay or the operating room, but a systematic and com­prehensive approach aids in the assessment of the trauma patient upon admission to the ICU and avoids missed or delayed diagnoses.

A i r w a y

A rapid assessment of the airway is necessary on arrival in the ICU. In the non-intubated patient, focus should be on a secure airway. The indications for an advanced airway are the same as in the trauma bay. Glasgow Coma Scale (GCS)
381
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D.J. Mancini et al.
of less than 8 from head injury or medications, signifi cant facial fractures, bilateral mandible fractures with loss of posterior tongue support, neck swelling from injury, or evi­dence of inhalational airway injury should all prompt consid­eration for immediate intubation upon arrival to the ICU.
In the intubated patient, confi rmation of a secure airway is essential. Endotracheal tubes are at risk for dislodgement or malposition (right main stem intubation or supraglottic posi­tioning) during transfer to ICU. All intubated patients should have a chest x-ray performed upon arrival in the ICU. Rapid assessment of type and size of endotracheal tube, listening for bilateral breath sounds, and confi rmation of end tidal CO
2
should also be completed. Endotracheal tubes need to be secured with either a well-positioned tube holder or tape, while a bite block can aid in the prevention of tube obstruc­tion. Early and frequent deep endotracheal and oral nasopha­ryngeal suctioning can prevent atelectasis caused by heavy secretions of blood or mucous. Restraints should also be employed to avoid self-extubation.

Breathing

Auscultation of breath sounds, if not completed during the airway assessment, is an essential part of the breathing assess­ment. Unequal breath sounds prompt an immediate response in a search for the cause. Endotracheal tube malposition or pneumothorax is the most common cause. If hemodynamic instability is present, needle thoracostomy is performed with a 14 g needle either in the second intercostal space along the midclavicular line or in the anterior axillary line at the fourth intercostal space in order to relieve the tension pneumothorax [ 2 ]. In the hemodynamically stable patient, pneumothorax may be diagnosed with chest x-ray or ultrasound evaluation of the pleural space [ 3 ]. An occult pneumothorax not identi- fi ed in the trauma bay may become apparent after the patient has been intubated and placed on positive pressure ventila­tion. Pneumothorax should be suspected in intubated patients with hypoxia and a sudden decrease in tidal volumes or increase in peak airway pressures.
Upon arrival to the ICU, all intubated patients should have continuous pulse oximetry monitoring implemented and an arterial blood gas drawn with consideration for place­ment of an arterial line if one has not already been placed. Initial ventilator settings should have a tidal volume set at 8 ml/kg or less, a respiratory rate set to the minute ventilation at 10 L/min, and positive end-expiratory pressure (PEEP) of 5 mmHg [ 4 , 5 ]. If the patient presents with signifi cant hypoxia or hypercapnia, an immediate cause should be identifi ed.
Early hypoxia in the trauma patient could be caused by endotracheal tube malposition, pneumothorax, pulmonary contusions, pulmonary embolism, or transfusion-related
lung injury (TRALI) [ 6 ]. The underlying cause should be addressed, but adjuncts including increasing the inspired oxygen concentration or increasing the PEEP on the ventila­tor can be used.
Hypoventilation and hypercapnia can result from overse­dation and depressed respiratory rate, inadequate pain con­trol causing splinting and decline in tidal volumes, or a central cord injury with denervation of the muscles of respi­ration. In both the non-intubated and intubated patients, the initial response should be directed at correcting the underly­ing cause. If the severity of the injury leading to the hypoven­tilation cannot be overcome in the non-intubated patient, then ventilatory support in the form of BiPAP or intubation must be considered.

Circulation

Initial assessment of circulation involves assessment of cir­culating blood volume, cardiac function, and vascular tone. Continuous ECG monitoring and an initial blood pressure should be obtained on admission to the intensive care unit. All trauma patients do not require invasive blood pressure monitoring, but an arterial line can be useful as monitoring adjunct in the patient with abnormal hemodynamics or the patient who will have frequent blood draws.
Adequate vascular access should be ensured. Two 18 g or larger intravenous lines should be used. If this is not possi­ble, then central vascular access should be obtained. In patients requiring ongoing blood product resuscitation, this should be a high-volume cordis line and not a long triple­lumen catheter. Any central line access placed emergently in the trauma bay should be considered for removal and new placement within 24 h [ 7 ]. These trauma lines should not be changed over a wire. If intraosseous lines were used for emergency access in the patient, they should be removed and more stable access obtained within the fi rst 24 h [ 7 ].
Any derangement in heart rate or blood pressure should be thought to be secondary to hypovolemic shock and ongo­ing hemorrhage until proven otherwise. Even in patients with normal vital signs but presenting to the ICU with new agita­tion or mental status changes, a high suspicion for bleeding must be maintained.
Ongoing bleeding when present should be corrected surgi­cally, either by returning to the OR or by bedside procedures if possible. On occasion the trauma patient is brought from the OR after a damage control procedure and remains cold and coagulopathic. Although the transfusion trigger for most chronic ICU patients is hemoglobin level of <7.0 g/dL, this does not apply to the trauma patient in the active resuscitation phase. In the immediate aftermath of hemorrhage, hemoglo­bin levels may be normal as equilibration has not occurred and the hemoglobin and hematocrit levels have not declined yet. In
33 Trauma
383
the acute setting, it is imperative to continue with a hemostatic resuscitation of blood products in a 1:1:1 ratio [
8 , 9 ]. Early
administration of FFP and platelets, within the fi rst 3 h after injury, has been shown to improve survival [
1012 ]. Patients
may also have been given TXA (tranexamic acid) as part of a massive transfusion protocol. This is typically given as a one­time dose of 1 g followed by another 1 g given over 8 h [
13 ,
14 ]. Massive transfusion is defi ned as transfusion of greater than ten units of pRBC [ 15 , 16 ]. Many centers now have a massive transfusion protocol (MTP) in place that streamlines the delivery of blood products by providing them from the blood bank in a fi xed ratio in continual fashion until the MTP is turned off. Much of this comes from the concept of damage control resuscitation that arose out of the military experience and involves permissive hypotension prior to surgical control of bleeding, 1:1:1 resuscitation with packed red blood cells (pRBC)/fresh frozen plasma (FFP)/platelets along with limit­ing total crystalloid infusion [ 17 , 18 ]. Implementation of this technique hopefully allows for avoidance of acute trauma coagulopathy. Clearly a marker of injury severity, once a patient has received over 20 units of pRBC during the resusci­tation, their risk of mortality increases to 50 % [ 19 ]. There is no cutoff point for the number of blood transfusions during the fi rst 24 h above which 100 % fatality is seen and further trans­fusion would be futile [ 20 , 21 ].
If hypovolemia and hemorrhage are not the cause of the patient’s hemodynamic derangements, then the presence of other shock states including cardiogenic, obstructive, and dis­tributive is assessed. Cardiogenic shock may result from myocardial ischemia or blunt cardiac injury. Blunt cardiac injury (BCI) will rarely cause hemodynamic instability and arrhythmias are more common. Any patient with blunt force mechanism to the sternum should be suspected to have sus­tained a BCI. These patients should have an electrocardio­gram (ECG) performed and be monitored with continuous ECG. If the ECG and troponin are negative, then BCI can be effectively ruled out [ 22 ]. Right ventricular dysfunction may result from BCI and is responsive to volume infusion and ionotropic support if needed. Myocardial ischemia or new valvular dysfunction requires immediate attention. The con­tinuous ECG monitor is insensitive to ST segment changes, and a 12-lead ECG better delineates changes suggestive of ischemia. Troponins and cardiac enzymes further aid in the diagnosis. A bedside cardiac ultrasound performed by the ICU provider rapidly assesses for ventricular function, valvu­lar competence, fi lling, and volume status [ 23 ]. Abnormalities discovered, especially from ventricular function and valvular disease, are rapidly addressed, and a confi rmatory formal car­diac transthoracic echocardiogram is obtained.
Obstructive shock can be secondary to cardiac tamponade or tension pneumothorax. Chest x-ray, focused transthoracic cardiac ultrasound, and clinical exam can point to these as causes for the shock state. Distributive shock in the trauma
patient is frequently secondary to neurogenic shock from a high spinal cord injury. Septic shock on presentation is rare in the trauma patient but should be considered as mortality is directly related to timing of broad spectrum antibiotics and source control [
24 ]. The severely injured multisystem trauma
patient may present with systemic infl ammatory response syndrome (SIRS) not secondary to infection but to the pro­infl ammatory state induced by the multisystem trauma [ 25 ].
There are several endpoints of resuscitation that may be used to guide treatment in the trauma patient. Standard hemodynamic parameters such as heart rate and blood pres­sure do not adequately quantify the physiologic defi cit in trauma patients. Base defi cit and serum lactate concentra­tions from an arterial blood gas analysis can identify patients in need of ongoing resuscitation. Persistent elevations in lac­tate or base defi cit could indicate ongoing hemorrhage or other complication [
1 ].

Disability

The initial assessment of the patient in the ICU involves obtaining a GCS (Table 33.1 ) and a quick neurologic assess- ment including pupillary refl ex and motor and sensory exam. Pupils are assessed for size, symmetry, and reactivity. Motor examination involves assessment of strength and movement in both the upper and lower extremities. Evaluation of sensory defi cits and levels becomes especially important in patients with suspected spine injuries. The motor and sensory exam should be obtained if possible prior to the administra­tion of medications that could impede the ability to obtain a reliable exam. Any new depression or change in mental sta­tus in a patient with a known intracranial hemorrhage should prompt rapid evaluation, contact with neurosurgical team, and consideration for repeat head CT [ 26 ]. Short-acting sed-
Table 33.1 Glasgow Coma Scale
Eye opening (4) Spontaneous 4
To command 3 To pain 2 None 1
Verbal response (5) Oriented 5
Confused 4 Inappropriate words 3 Incomprehensible 2 None 1
Motor response (6) Follows commands 6
Localizes to pain 5 Withdrawals to pain 4 Flexion (decorticate posturing) 3 Extension (decerebrate posturing) 2 None 1
Total 3–15
384
D.J. Mancini et al.
ative and pain medications are utilized to preserve the ability for a clinical neurologic exam with pause in the medication administration. Throughout the patient ICU course, close communication with the neurosurgical team is essential.

Environment/Exposure

Temperature of the patient is a critical element in the initial assessment. Central temperature monitoring with Foley tem­perature probe or esophageal temperature probe provides the most accurate assessment. Prevention of hypothermia (<35 °C) is the initial goal for the trauma patient presenting to the ICU. Open abdomens, large burn surface area, and prior exposure all contribute to heat loss. Patients will at times present severely hypothermic (<32 °C). This level of hypothermia results in decreased platelet adhesion, impaired cardiac function from increased systemic vasoconstriction, frequent dysrhythmias from myocardial irritability, and impaired clotting factor function. In patients who have suf­fered a cardiac arrest that led to their trauma, consider imple­menting the postarrest hypothermic protocol using 36 °C instead of 34 °C as the goal temperature [ 27 ].
A search for unidentifi ed wounds should be undertaken as part of the initial assessment of the trauma patient in the ICU. If wounds are found, they are thoroughly examined and decisions on further workup and closure of the wounds are made. If the wound is in proximity to a joint or fracture site, the possibility of an open fracture or violation of the joint space should be entertained.

Early and Later Stages of ICU Care

Once the initial assessment of the trauma patient is complete, an organ system approach to ICU care for the patient is useful. This is utilized in both the early stage (fi rst 72 h, resuscitation and early support phase) and the later stage (after 72 h, late support and recovery phase) of ICU care. It allows for a complete assess­ment of the trauma patient and minimizes missing issues that could affect outcome. During this stage of ICU care, the patient will either progress toward recovery and discharge from the ICU, worsen signifi cantly due to complications and multisys­tem organ dysfunction, or plateau and remain chronically criti­cally ill. Which path the patient takes is dictated by their burden of injury but also by the quality of ICU care they receive.

Neurologic

In the early stage of ICU care of a patient with a neurologic injury from traumatic brain injury (TBI) or spinal cord injury, focus is on prevention of secondary neuronal injury by
avoidance of hypotension and hypoxia. Hyperglycemia, hypercarbia, and hyperthermia can also worsen neurologic injury. Minimizing sedative use and narcotics in this early stage allows for a reliably neurologic exam. In patients with­out a reliable neurologic exam, placement of intracranial pressure monitors or ventriculostomies is often necessary. Close and frequent communication with a consulting neuro­surgeon is mandatory.
The guiding principle for care of the patient with TBI is maintenance of cerebral perfusion pressure (CPP). The CPP equals the mean arterial pressure (MAP) minus the intracra­nial pressure (ICP), CPP = MAP − ICP. To keep the injured brain well perfused, a goal CPP >60 mmHg is maintained through manipulation of ICP or MAP. The goal ICP is <20 mmHg. Maneuvers to decrease ICP include elevation of the head of the bed to greater than 30° to promote drainage of cerebrospinal fl uid (CSF) and loosening cervical collar to relieve pressure on the jugular venous system. In the acute setting, hyperventilation can be utilized to decrease ICP through cerebral vasoconstriction. TBI patients should be kept within a normal range for CO 2 , 35–40 mmHg, as both persistent hypo- and hypercarbia are detrimental. Mannitol (1 g/kg) or hypertonic saline can both be used for acute ICP elevations. Normothermia can be maintained with acetamin­ophen and cooling blankets and adequate sedation provided in order to decrease metabolic demand. Phenobarbital­induced coma and paralysis are utilized for refractory ICP elevations until defi nitive treatment with decompressive cra­niotomy can be performed. Adequate MAP is essential in patients with TBI. The fi rst step is to ensure euvolemia. Mannitol acts as an osmotic diuretic and can lead to hypovo­lemia without fl uid resuscitation. Once euvolemia is achieved, further fl uid resuscitation can be harmful, and vasopressor therapy with an agent such as phenylephrine may be necessary. Phenylephrine has minimal effects on cerebral blood vessels and is the agent of choice to raise MAP in patients with TBI.
Injury to the spinal cord and protection of the cervical spine can signifi cantly complicate the care of injured patient in the ICU. Frequently associated with high thoracic or cer­vical spinal cord injuries, neurogenic shock is related to loss of sympathetic tone. As in TBI once euvolemia is assured, further fl uid resuscitation becomes detrimental. The vasodi­lation secondary to neurogenic shock can be treated with vasopressors such as phenylephrine or norepinephrine. Cervical spine injury can also lead to decreased cardiac inot­ropy and chronotropy. Atropine and possibly emergent car­diac pacing in patients with refractory bradycardia may be necessary. In patients with traumatic brain injury or spinal cord injury, hypotension must be avoided.
Cervical spine clearance in the ICU is made more diffi cult in cases of patient obtundation, agitation, or sedation. Options to clear the cervical spine in persistently obtunded
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385
or comatose patients without the possibility of reliable clinical exam include CT alone, MRI, or simply leaving the collar in place [
28 ]. There is no role for fl exion-extension
fi lms in clearance of the cervical spine in the obtunded ICU patient. Each institution should develop an agreed upon and adhered to policy for cervical spine clearance in the obtunded patient.
Pain control is important throughout a patient’s hospital course from the initial presentation through to discharge and rehabilitation. Pain assessment can best be accomplished with a visual or numerical pain scale. Analgesic medications are chosen based on their onset and duration of action. In the intubated patient, a continuous infusion may be needed.
Most, but not all, intubated patients will require sedative medications. In the early stages of ICU care, propofol can be an excellent medication for this purpose because of its fast onset and clearance. Continuous infusion of propofol is lim­ited by hypertriglyceridemia and the concern for propofol infusion syndrome [ 29 ]. Alternative sedative medications may be given such as benzodiazepines. Benzodiazepines are ideally given as intermittent medications but at times a con­tinuous infusion is required. These medications can have a signifi cant volume of distribution and thus take an extended amount of time to wash out of the system after discontinua­tion. Benzodiazepines may also contribute to ICU delirium, especially in the elderly. Delirium in the trauma patient can be diffi cult to manage as care is required that patients do not harm themselves and the diagnosis can be clouded by TBI or withdrawal. Delirium management is the same as in other patient populations with discontinuation of possible inciting medications, reorientation, maintaining normal sleep-wake cycles, and judicious use of typical or atypical antipsychotic medications [ 30 ].
Withdrawal from alcohol or drugs is a common problem in the trauma population. Over 70 % of trauma patients will present intoxicated [ 3133 ]. Patients who report a signifi cant alcohol or drug use history are also at risk for withdrawal. Withdrawal often does not present until 48–72 h after admis­sion and can be initially masked by administration of propo­fol and benzodiazepines in the early stage of ICU care.
In the later stage of ICU care, TBI rehabilitation and dis­position plans coalesce. Work with physical and occupa­tional therapy begins as early as feasible, and disposition planning is a multispecialty endeavor incorporating input from all of the consulting services, nursing, physical and occupational therapy, and social work.

Pulmonary

The early stage of ICU care for patients with respiratory fail­ure revolves around prevention of secondary complications and diagnosis and treatment of the underlying cause of the
Table 33.2 Ventilator-associated pneumonia prevention bundle
Elevation of the head of bed to at least 30° Daily mouth care with 0.12 % chlorhexidine mouthwash Stress-related gastrointestinal ulcer disease prophylaxis Deep venous thrombosis prophylaxis Daily sedation pause for assessment of readiness to extubate
respiratory failure. Once immediate issues pertaining to breathing and the pulmonary system are addressed on the initial assessment, attention is directed at mechanical venti­lation management with the goal to resolve the underlying cause of the patient’s respiratory failure and ventilator libera­tion. All mechanically ventilated are placed on a ventilator­associated pneumonia prevention bundle (Table 33.2 ) [ 34 ].
Hypoxia and possible respiratory failure result from conditions such as pulmonary edema secondary to pulmo­nary contusions or cardiac failure, aspiration pneumonitis, pneumonia, acute respiratory distress syndrome (ARDS), TRALI, and pulmonary embolism. Pulmonary contusions after blunt torso trauma cause parenchymal cellular destruc­tion and alveolar space fl ooding with blood and debris. Large contusions may lead to a signifi cant shunt and severe hypoxia. Treatment ranges from noninvasive to aggressive and invasive. Options include elevating PEEP to keep via­ble alveoli open and frequent pulmonary toilet maneuvers and suctioning to clear large airways. Advanced techniques include independent lung ventilation for unilateral injuries to limit barotrauma to unaffected lung and extracorporeal membrane oxygenation (ECMO). Similar to the fl ooding of alveolar spaces with blood and debris is pulmonary edema caused by acute fl uid overload from aggressive resuscita­tion or cardiac failure after blunt cardiac injury or myocar­dial infarction. Transfusion acute cardiac overload (TACO) after large- volume blood transfusion also presents with pulmonary edema. TACO has been shown to occur in around 2 % of ICU patients who have received blood prod-
35 ]. Treatment of the pulmonary edema includes opti-
ucts [ mization of cardiac output with inotropes and possible diuresis to decrease afterload. Consider noninvasive moni­toring with devices that measure stroke volume or pulse pressure variation or invasive cardiac output monitoring with a pulmonary artery catheter or bedside continuous transesophageal echocardiography to better optimize fl uid status.
ARDS is defi ned by fl uffy infi ltrates on chest radiograph, the presence of an inciting event such, and hypoxia. The degree of hypoxia is measured by the PO
/FIO 2 ratio. Mild
2
ARDS is defi ned as PO 2 /FIO 2 < 300, moderate ARDS PO 2 /
< 200, and severe ARDS PO 2 /FIO 2 < 100 [ 36 ]. Trauma
FIO
2
patients who have received a massive transfusion or have evidence of aspiration are at particular risk for developing ARDS [ 37 ]. Most patients who suffer aspiration have a
386
D.J. Mancini et al.
chemical pneumonitis and do not require empiric antibiotic therapy [
38 ]. Antibiotics should be reserved for patients who
demonstrate a bacterial source for their pneumonia.
Pulmonary embolism (PE) is unlikely during early ICU care, but should be considered in the hypoxic, tachycardic, and tachypneic patient. Patients with intracranial, spinal cord, mul­tiple long bone, or pelvic injuries have been found to have deep venous thrombosis (DVT) rates up to 80 % without chemopro­phylaxis and should be started on chemical DVT prophylaxis when injuries permit [Barrera]. While chest radiographs are often normal in appearance, an arterial blood gas may show a respiratory alkalosis with a signifi cant A-a gradient. A 12-lead ECG most commonly is signifi cant for sinus tachycardia and rarely shows the S1 Q3 T3 pattern indicative of right heart strain. A focused transthoracic cardiac ultrasound can be effec­tive at identifying septal bowing, apical right ventricle, and right ventricular dilation, all signs of right heart strain and pos­sibly a large PE [ 39 ]. D-dimer determination is unhelpful in the diagnosis of PE in the acutely injured patient. Defi nitive diag­nosis can be made by contrast computed tomography of the chest utilizing a specifi c pulmonary embolism protocol. Ventilation perfusion scans may be considered in cases where the patient cannot receive IV iodinated contrast material. Initial treatment for PE is anticoagulation with heparin or low-molec­ular-weight heparin. Although patients reach therapeutic anti­coagulation faster on low-molecular-weight heparin, an IV drip of heparin is preferred in the trauma patient at high risk of bleeding as the drip is easily stopped. Inferior vena cava (IVC) fi lters may be utilized in patients with pulmonary embolus and contraindication to anticoagulation or who develop a PE while therapeutically anticoagulated [ 40 ].
Other less frequent causes of hypoxia include fat embo­lism syndrome and transfusion-related lung injury (TRALI). Fat embolism syndrome most often occurs during manipula­tion of long bone fractures and femur fi xation by intramedul­lary rodding. Signs include hypoxemia, mental status changes, and upper extremity cutaneous petechiae [ 41 ]. The diagnosis is one of exclusion and treatment is largely sup­portive. TRALI is an uncommon, idiosyncratic reaction to blood transfusion that can cause acute hypoxemia and respi­ratory failure. The incidence of TRALI in ICU patients receiving blood is 0.5 % [ 35 ]. Treatment is directed at stop- ping the transfusion and respiratory support.
Hypoventilatory respiratory failure results from altered mental status secondary to TBI or over sedation, chest wall injury, spinal cord injury, and intra-abdominal hypertension. For the obtunded or sedated, treatment is aimed at correcting the underlying cause of obtundation, decreasing sedation, or reversing narcotics. Obtundation from narcotics must be bal­anced with adequate pain control in patients with chest wall injuries. Rib fractures and chest wall contusions often cause signifi cant pain, inhibit respiratory mechanics, and ulti­mately decrease minute ventilation.
Several methods of pain control are effective at treating chest wall pain. A thoracic epidural containing a local anes­thetic, with or without a narcotic additive, has been shown to be effective in improving pain control in patients with chest wall pain from rib fractures [
42 ]. In patients with thoracic
narcotic-containing epidurals, it is important to note that epi­dural narcotics may cause systemic effects including depressed mental status and decreased minute ventilation. Systemic narcotics via a patient-controlled anesthesia (PCA) can also be effective at treating chest wall injury pain but have an even greater risk of mental status and respiratory depression. Local nerve blocks of the intercostal nerves asso­ciated with fractured ribs may also provide temporary pain relief [ 43 ].
Spinal cord injury above C3–5 obliterates diaphragm function, often necessitating early intubation in the patient with a cord injury at this level. Cord injury in the lower cervi­cal and high thoracic region can also compromise ventilation through loss of accessory muscles such as the intercostals and sternocleidomastoids. This typically presents later in the ICU course that may lead to delayed respiratory failure from a tired, overburdened diaphragm or from increased work of breathing from the now denervated stiff muscles of the chest wall [ 44 ]. Exaggerated abdominal breathing is one indica- tion of impending respiratory failure and early controlled intubation is recommended.
Another important consideration in the critically injured patient with hypoventilation is abdominal compartment syn­drome (ACS). This constellation of symptoms includes hypotension, oliguria, and increased peak airway pressures. Plateau pressures on the ventilator are often unchanged in ACS. Increased abdominal volume from bleeding, ascites, or bowel edema after an aggressive resuscitation may lead to an increased pressure on the diaphragm and a decreased tidal volume. ACS is relieved by laparotomy and abdominal decompression.
Once the processes driving respiratory failure have been addressed, attention turns to ventilator liberation. Several factors can limit the ability to liberate from the ventilator in the trauma patient. Mental status, either depressed or agi­tated, can make decreasing ventilator support diffi cult. Care should be taken in the TBI patient that ventilator liberation will not result in hypercarbia or hypoxia. Increased pain with emergence from sedation and continuous pain medications can impair the ability to take adequate tidal volumes due to splinting.

Cardiovascular

A patient’s injuries may result from a motor vehicle colli­sion, fall, or other trauma but the reason for the car crash or the fall is often unknown. A high index of suspicion,
33 Trauma
387
especially in the elderly patient population, of a cardiac cause for the fall should be maintained. A syncope workup includes a careful history and physical exam, ECG, cardiac enzymes, echocardiogram, as well as a review of the patient’s medications to discover any potential causes [
45 ]. Close
review of a patient’s outpatient medications and contact with their primary care provider early in their ICU course aids in the discovery of underlying medical problems and accurate medication dosing. Particular attention is required in the elderly patient population. Pre-existing arrhythmias, hyper­tension, and myocardial ischemia can complicate the patient ICU course. Patients should be returned to their home medi­cation regimen as soon as possible. The patient’s condition and ongoing resuscitation efforts can make this diffi cult. Remain aware that patients on beta blockade may not mount a tachycardic response to hypovolemia and can cloud the clinical picture.
Certain traumatic injuries require more aggressive blood pressure management. Traumatic aortic disruption in the tho­racic aorta is often repaired with a stent graft. In the stable patient, this can be done within the fi rst 48 h after injury [ 46 ]. During that time tight heart rate and blood pressure control is mandatory. The target heart rate of <80 bpm can be achieved with beta blockade or an infusion of esmolol or labetalol. The target systolic blood pressure of <120 mmHg is obtained with nicardipine or labetalol in a continuous infusion if needed. Hydralazine, a potent vasodilator, does not allow for the fi ner control the other agents offer and is not recommended.

Renal/Electrolytes

Acute kidney injury (AKI) is a common occurrence in trauma patients and is best treated with prevention. Estimates of the incidence of AKI in trauma patients range from 6.3 to 27 % and risk factors are listed in Table 33.3 [ 47 ]. The tradi- tional division of AKI into pre-, post-, and intrarenal is not a classifi cation system but is useful for thinking about causes. If left uncorrected both prerenal and postrenal AKI will result in intrarenal AKI.
Table 33.3 Risk factors for acute kidney injury
Shock Sepsis Age >65 years Burns Rhabdomyolysis Pre-existing chronic kidney injury Pre-existing cardiovascular disease Exposure to nephrotoxins: radiocontrast material, aminoglycosides Abdominal injuries Need for mechanical ventilation
Prerenal AKI is a consequence of renal hypoperfusion. Maintenance of euvolemia is essential for the prevention of AKI. The early stage of resuscitation of the trauma patient in hemorrhagic colloids in the form of blood products with the minimization of crystalloids has been shown to be benefi cial. Once resuscitated maintenance fl uids in the form of Ringer’s lactate or Plasma-Lyte can be used. Later in the ICU course, care is required to keep up with a patient’s losses from the gastrointestinal tract, in the form of stool and naso- or oro­gastric tube output, wound evaporative losses, as well as losses via a V.A.C. dressing on the abdomen. Once euvolemia is assured, norepinephrine may be used for maintenance of vascular tone and arterial blood pressure as it has been shown to augment renal blood fl ow [ 47 ].
Postrenal AKI results from an obstruction downstream from the renal collecting system. In trauma patients this obstruction usually stems from a blockage of urinary cathe­ter drainage by clot or malposition. External compression, iatrogenic surgical ligature, edema, urethral injury, and intrinsic stricture are other possible causes of postrenal AKI in the trauma patient.
Intrarenal or intrinsic AKI stems from impairment of the renal tubular collecting system. Prolonged renal hypoperfu­sion due to shock remains the most common cause of intrin­sic AKI. Sepsis, rhabdomyolysis, nephrotoxic agents, as well as hyperchloremia from overuse of 0.9 % NaCl also pre­cipitate intrinsic AKI. AKI that occurs in the early stage of ICU care is most likely attributable to the patient’s trauma and subsequent hypoperfusion; later onset AKI is more likely secondary to sepsis. Patients who have received intra­venous contrast for CT scan as part of the initial trauma workup have a theoretical risk of increased AKI. Some stud­ies have suggested that intravenous contrast from the initial CT scan does not increase the likelihood of developing AKI [ 48 , 49 ].
Management of new-onset AKI involves maintenance of euvolemia, avoidance of hypervolemia, and cessation of renal toxic agents. Urinalysis, urine electrolyte studies, and examination for urine casts along renal consultation should occur early in the course of AKI. Initiate renal support in the form of hemodialysis or hemofi ltration early. Indications for dialysis include acidosis, severe electrolyte abnormalities, volume overload, and uremia. Subclavian access for hemodi­alysis lines should be avoided to prevent stenosis and pre­serve future access options.
Electrolyte disorders are common in the ICU trauma patient. Alkalosis, high circulating catecholamine concentra­tions, hypothermia, use of osmotic or loop diuretics, antifun­gal medications, and exogenous steroids all cause hypokalemia. Potassium levels are monitored and replaced with intravenous potassium. Hyperkalemia is often second­ary to acidosis, rhabdomyolysis or crush injuries, large­volume blood transfusions, or AKI. Hypocalcemia in the