Trauma

C. spontaneous eye opening The incidence of severe head injury remains high despite the enactment of various laws mandating protective devices (eg, seatbelts, airbags, motorcycle and bicycle helmets) and ongoing educational efforts. In addition to the devastating emotional and social toll, the economic consequences are daunting. The identification of accurate and objective criteria for the early prediction of long-term survival thus becomes increasingly important. Recent studies have demonstrated the accuracy of several clinical parameters in the formulation of prognostic assessments during the initial 24 hours after head injury. There appears to be a nearly perfect linear relationship between increasing age and diminishing survival. This factor is significantly predictive at both initial evaluation and 24 hours post injury. The same appears to be true for best motor score and presence of pupillary activity to light, although the relationship is not as strong. Extraocular motility is significant at 24 hours but not at the initial admission evaluation. Spontaneous eye opening, an important factor in the determination of the Glasgow coma scale and thus of interval changes in the level of coma, does not appear to be a reliable factor for survival prediction, at least not during the initial 24 hours after injury. These factors may be useful in survival prognostications, but they are not definitive. They merely suggest an increasingly or decreasingly favorable outcome, but should not be used to define survivability for any individual patient.

During the initial 24 hours after severe head trauma, factors useful in predicting survival include all of the following EXCEPT: A. extraocular motility B. age C. spontaneous eye opening D. pupillary activity E. best motor score

C. electrocardiography The diagnosis of cardiac contusion resulting from blunt injury is based on several tests developed for evaluation of nontraumatic cardiac disease—MB-fraction serum creatinine phosphokinase (CPK-MB) levels, radioisotope scanning of several types, and cardiac ultrasound examination (echocardiography)—as well as the electrocardiogram. A rash of studies over some years based chiefly on serum enzyme levels or imaging studies suggested that cardiac contusion was much more common than previously believed, and formal and aggressive cardiac monitoring became almost routine for patients with blunt injury. It has become apparent that untoward cardiac events actually occur in only 3% to 4% of such patients. The complication is an arrhythmia in most cases. A number of recent investigations have concluded that screening of blunt injury patients for possibly significant cardiac contusion can be much simplified and that cardiac monitoring can be limited. The two diagnostic studies that relate to clinically significant myocardial contusion are electrocardiogram and CPK-MB. Because arrhythmia is the abnormality manifested in most patients with cardiac contusion, an electrocardiogram is much more specific than CPK-MB and is the best initial screening test for these patients. Radionuclide scanning is not useful for evaluating whether blunt injury patients have cardiac contusion. Echocardiography may be of some value in following the course of a known contusion, but is not required for initial screening. Computed tomography should not be used for this purpose.

The best initial screening test for cardiac contusion after blunt injury is: A. MB-fraction serum creatinine phosphokinase (CPK-MB) determination B. echocardiography C. electrocardiography D. computed tomography E. radioisotope scanning

E. placement of an intracranial pressure monitor The most important aspects of care in the head-injured patient are avoidance of hypoxia and hypotension; a single episode of systolic blood pressure <90 mmHg doubles mortality, while a PAO2 <60 mmHg is an independent predictor of poor outcome. This patient has been intubated for both mechanical airway protection and control of hypoxia. Cerebral blood flow (CBF) correlates roughly with cerebral perfusion pressure (CPP), which depends on systemic and intracranial pressure (ICP): CPP = mean arterial pressure (MAP) - ICP. Maximizing CPP is important, as intracranial hypertension may cause herniation or ischemia. Furosemide and mannitol, meant to reduce brain parenchymal swelling and ICP, cause diuresis and may result in significant hypotension; mannitol may be used for proven high ICP but should be avoided in hypotensive patients. Hypertonic saline solution can reduce ICP, but treatment goals cannot be evaluated without intracranial ICP monitoring. CBF may be especially depressed immediately after injury; thus hyperventilation, which causes vasoconstriction and thus decreases CBF, may be more hazardous early in the patient's course. Any patient with Glasgow Coma Scale (GCS) score ≤8 and demonstrated intracranial pathology should have an ICP monitor placed for optimization of CBF and ICP.

A 20-year-old man with an isolated closed head injury secondary to a baseball bat blow comes to the emergency department on a backboard with a cervical collar in place. His Glasgow coma scale score is 6, he has been intubated, and a CT scan shows bi-temporal subarachnoid blood without evidence of herniation. The next step in management should be A. administration of 100 mg of furosemide and 75 mg of mannitol intravenously B. hyperventilation to a PCO 2of 30 mm Hg C. hyperventilation to a PCO 2of 25 mm Hg D. administration of 100 ml of 25% hypertonic saline solution E. placement of an intracranial pressure monitor

E. intra-abdominal abscess The physiologic response to injury and secondary infection is characterized by a cascade of events that unchecked sets the stage for dysfunction in multiple organs. Physiologic impairment of the respiratory system is reflected by an increased capillary permeability with an associated decreased compliance and reduced arterial oxygen tension due to the resultant pulmonary edema. Early-onset renal dysfunction typically follows hypoperfusion, either due to acute hypovolemia or decreased cardiac output secondary to poor myocardial contractility. An episode of severe hypotension may also precede hepatic dysfunction, characterized by a prolonged prothrombin time and hypoglycemia. These clinical features are further accentuated in the presence of underlying liver disease. Altered mental status without localizing signs is particularly common, but may be difficult to distinguish from the primary injury if the patient has sustained head trauma or has severe cerebrovascular disease. Thrombocytopenia is a frequent hematologic abnormality in critical illness, and may represent a dilutional effect after large volume resuscitation as well as increased consumption (disseminated intravascular coagulation, DIC); intravascular sequestration; or impaired thrombopoiesis secondary to suppression of bone marrow function. Other subtle manifestations of underlying sepsis include insulin resistance, intolerance of enteral feeding, ileus, and anemia. If high-volume crystalloid infusions are required beyond the initial 48-72 hours after injury to maintain hemodynamic stability and urine output, a reason for failure of the inflammatory response to resolve should be sought. Similarly, the development of otherwise unexplained multiple organ dysfunction is a frequent harbinger of occult infection and should trigger an active search for a source. Although several infectious etiologies may produce the syndrome, a common source in the postsurgical patient is the abdomen, particularly if it was the operative site. Ultrasonography and computed tomographic (CT) scans can usually help to establish the presence or absence of a significant intra-abdominal lesion, but are less reliable for the diagnosis of anastomotic leak with minimal spillage or gut ischemia. Celiotomy undertaken in a deteriorating patient despite negative radiologic evidence remains controversial. Proponents argue that the rate of positive findings may be as high as 60%. Opponents counter that the prognosis for such patients remains poor, even if the problem is treated. "Treatment" of suspected occult infection with empirical broad-spectrum antibiotics alone should be avoided.

A 25-year-old male pedestrian has a closed head injury, a pulmonary contusion, an open pelvic fracture, and blunt abdominal trauma after being hit by a car. Five days after celiotomy requiring splenectomy, he is receiving crystalloids (250 mL/hr) to maintain urine output above 2 mL/kg/hr and systolic blood pressure above 70 mm Hg. His laboratory values are as follows: hematocrit, 24%; WBC count, 4,500/cu mm; platelet count, 40,000; prothrombin time (PT), 20 sec (control, 12 sec); partial thromboplastin time (PTT), 60 sec (normal, 30 to 40 sec); BUN, 45 mg/dL; creatinine, 2.1 mg/dL; and fibrinogen, 200 mg/dL. The most likely explanation for these abnormalities is: A. transfusion reaction B. hemolytic-uremic syndrome C. diabetes insipidus secondary to head injury D. disseminated intravascular coagulation E. intra-abdominal abscess

E. orotracheal intubation with in-line stabilization Care of the head-injured patient begins with assessment of the severity of injury and protection of the brain from further insult. Outcome depends on recognition, severity, and treatment of two fundamentally distinct types of head injury: diffuse and focal. The importance of the initial assessment of the head-injured patient cannot be overemphasized, because it forms the basis for sequential reassessment and subsequent treatment decisions. Rapid neurologic evaluation is a critical component of the primary survey and is performed immediately after control of airway, breathing, and circulation. This evaluation assesses the patient's level of consciousness as alert, responsive to verbal stimuli, responsive to painful stimuli, or unresponsive (the AVPU method). The minineurologic examination that follows in the secondary survey should repeatedly assess the Glasgow coma scale, pupillary function, and lateralized extremity weakness. Abnormalities of all three of these components generally indicate a focal mass lesion, such as subdural, epidural, or intracerebral hematoma. Subdural hematoma is the most common, occurring in 20% to 40% of severely head-injured patients. The combination of progressive hypertension associated with bradycardia and a diminished respiratory rate (the Cushing response) strongly suggests a rise in intracranial pressure due to a mass lesion. Glasgow coma scale abnormalities without pupillary change or lateralized extremity weakness may signify diffuse brain injury, in particular, diffuse axonal injury, concussion, or hypoxemia. Bleeding into the subarachnoid space is characterized by a depressed level of consciousness, severe headache, or photophobia. The Glasgow coma scale is a global measure of brain dysfunction. Although it may be altered not only by head injury but also by hypotension, hypoxemia, and ingestion of neurologic depressants, it contains considerable prognostic information and allows classification of head injury as mild (13-15), moderate (9-12), or severe (8 or less). Patients with severe head injuries should have immediate establishment of an endotracheal airway with manual in-line stabilization and high flow oxygen as the first step in management to prevent further brain insult from hypoxia. Hypotension should be corrected by fluid resuscitation and should never be presumed to be the result of brain injury.

A 30-year-old man is admitted after a motor vehicle crash. His blood pressure is 180/60, pulse rate is 65/min, and respiratory rate is 25/min. His level of consciousness is markedly depressed, with unequal pupillary response and extensor posturing on the right side. The first step in the management of this patient should be: A. high flow oxygen via a face mask B. immediate computed tomographic (CT) scan to localize a mass lesion C. placement of large peripheral intravenous lines and rapid infusion of mannitol D. bilateral bur holes and attempted clot evacuation E. orotracheal intubation with in-line stabilization

E. An acute subdural hematoma Care of the head-injured patient begins with assessment of the severity of injury and protection of the brain from further insult. Outcome depends on recognition, severity, and treatment of two fundamentally distinct types of head injury: diffuse and focal. The importance of the initial assessment of the head-injured patient cannot be overemphasized, because it forms the basis for sequential reassessment and subsequent treatment decisions. Rapid neurologic evaluation is a critical component of the primary survey and is performed immediately after control of airway, breathing, and circulation. This evaluation assesses the patient's level of consciousness as alert, responsive to verbal stimuli, responsive to painful stimuli, or unresponsive (the AVPU method). The minineurologic examination that follows in the secondary survey should repeatedly assess the Glasgow coma scale, pupillary function, and lateralized extremity weakness. Abnormalities of all three of these components generally indicate a focal mass lesion, such as subdural, epidural, or intracerebral hematoma. Subdural hematoma is the most common, occurring in 20% to 40% of severely head-injured patients. The combination of progressive hypertension associated with bradycardia and a diminished respiratory rate (the Cushing response) strongly suggests a rise in intracranial pressure due to a mass lesion. Glasgow coma scale abnormalities without pupillary change or lateralized extremity weakness may signify diffuse brain injury, in particular, diffuse axonal injury, concussion, or hypoxemia. Bleeding into the subarachnoid space is characterized by a depressed level of consciousness, severe headache, or photophobia. The Glasgow coma scale is a global measure of brain dysfunction. Although it may be altered not only by head injury but also by hypotension, hypoxemia, and ingestion of neurologic depressants, it contains considerable prognostic information and allows classification of head injury as mild (13-15), moderate (9-12), or severe (8 or less). Patients with severe head injuries should have immediate establishment of an endotracheal airway with manual in-line stabilization and high flow oxygen as the first step in management to prevent further brain insult from hypoxia. Hypotension should be corrected by fluid resuscitation and should never be presumed to be the result of brain injury.

A 30-year-old man is admitted after a motor vehicle crash. His blood pressure is 180/60, pulse rate is 65/min, and respiratory rate is 25/min. His level of consciousness is markedly depressed, with unequal pupillary response and extensor posturing on the right side. Which of the following most likely explains these symptoms? A. A subarachnoid hemorrhage B. Diffuse axonal injury C. Herniation of the cerebellar tonsils D. Hypoxemia E. An acute subdural hematoma

C. ICP is >20. As brain injury worsens, there is increased parasympathetic and sympathetic activity secondary to increased brain swelling with ICP >20 usually. This decreases cerebral perfusion pressure (CPP). The body has a reflex, known as Cushing reflex, to compensate for this and is defined as increased systolic blood pressure (SBP), bradycardia, and slow irregular breathing.

A 35-year-old male is in the ICU intubated after sustaining a head injury due to a motorcycle crash. His heart rate decreases from 80 to 50, SBP is 160 mmHg, and his breathing becomes slowed and irregular. It is likely that: A. Brain swelling is decreasing. B. ICP (intracranial pressure) is <10. C. ICP is >20. D. Sympathetic nervous system has decreased activity. E. Parasympathetic nervous system has decreased activity.

C. aggressive pulmonary toilet, effective pain control, supplemental oxygen, and avoidance of overhydration A diagnosis of flail chest after blunt trauma requires that the treating physician continuously reevaluate the patient for signs and symptoms of respiratory compromise. In the absence of hemopneumothorax, tube thoracostomy is not required, although it may be deemed advisory if the patient is to receive positive-pressure ventilatory support, and especially if ventilatory support is needed for an operative procedure, when the patient would be covered by drapes and difficult to evaluate continuously. Over-hydration should be avoided because it may exacerbate pulmonary congestion and edema. In the absence of imminent respiratory failure, treatment must include aggressive pulmonary toilet, which is not possible without effective pain control. Tape wrapping and/or splinting should never be performed.

A 35-year-old man driving without a seat belt is brought to the emergency department after a crash in which the steering wheel was bent. There is no evidence of neurologic trauma and no evidence of hemodynamic instability. The chest x-ray reveals a normal-appearing mediastinum and multiple rib fractures on the left side, with evidence of a flail segment. There is no pneumothorax. Physical examination and a computed tomographic (CT) scan of the abdomen are normal. The patient's respiratory rate is 24/min and shallow, and arterial blood gases (40 per cent oxygen by face mask) are PaO2, 105 torr; PaCO2, 35 torr; and pH, 7.48. Management of this patient should include: A. tape wrapping to splint the flail segment B. left tube thoracostomy C. aggressive pulmonary toilet, effective pain control, supplemental oxygen, and avoidance of overhydration D. immediate endotracheal intubation E. cricothyroidostomy

B. diagnostic peritoneal tap/lavage Knowing priorities is key for optimal management of multiple trauma patients. A patient who is hemodynamically labile in the trauma setting has hemorrhagic shock until proven otherwise. With the exception of brisk bleeding from an open wound, three body cavities in which blood loss can result in hemodynamic lability are the chest, abdomen, and pelvis. Although this patient has several major problems, including a blown left pupil, a widened mediastinum, an unstable pelvic fracture, and a possible spinal cord injury, a systematic approach is imperative. This patient has been intubated and breath sounds are equal bilaterally, which is not consistent with a tension pneumothorax or massive hemothorax. The primary survey should emphasize the patient's circulatory status to determine the cause of his hemodynamic lability. With the chest cavity essentially ruled out for containing any significant blood loss, a diagnostic peritoneal tap/lavage (open, supraumbilical approach) would be the most expeditious method to determine the site of blood loss. The aspiration of nonclotting blood would be diagnostic for intra-abdominal bleeding and would dictate that the patient be taken to the operating suite for exploration. However, if the patient does not have gross blood on diagnostic peritoneal aspiration, angiography to identify the probable active arterial bleeding from the pelvic fracture should be considered. Embolization plays a pivotal role in the management of arterial bleeding from a pelvic fracture. In the hemodynamically labile patient, computed tomographic (CT) scan has no role in the evaluation of suspected abdominal injury. Immediate operation would be inappropriate unless there is confirmation of active intra-abdominal bleeding. This patient's clinical presentation is highly suggestive of an intracranial injury. Although he has a blown pupil, his hypotension should not be attributed to his head injury. Traumatic aortic disruption causes exsanguination and death, not hypotension. Although a cervical fracture could result in spinal cord injury and subsequent neurogenic shock, initial management to rule out a hemorrhagic source is still required.

A 41-year-old man is brought to a community hospital for stabilization prior to transport after a motorcycle crash. He is comatose and hemodynamically labile and is intubated translaryngeally. Breath sounds are equal bilaterally. A pelvic binder was applied in the field because of an unstable pelvic fracture and transient episodes of hypotension and he was given three units of packed red blood cells. After transport and with a fourth unit being infused, the patient has a systolic blood pressure of 90 torr. He has a blown left pupil, widened mediastinum, unstable pelvic fracture, and C3-4 subluxation. Initial management should be: A. computed tomographic scan of the head, abdomen, and pelvis B. diagnostic peritoneal tap/lavage C. immediate celiotomy D. angiographic embolization of a pelvic bleeding site E. a bur hole and emergency thoracotomy to repair traumatic aortic disruption

D. 2760 The most commonly used method for estimating the caloric needs of patients applies the Harris-Benedict equations. The basal energy expenditure (BEE) is calculated from the weight, height, and age of the patient. Once the BEE has been calculated, the total energy expenditure (TEE) must be calculated using estimates of the patient's physical activity and the extent to which the disease has induced hypermetabolism. TEE = BEE * (activity factor) * (stress factor). Some activity factors are: Patient on ventilator 1.10, Patient on bed rest 1.15, Normal ambulation 1.25, Manual worker 1.50-2.00, The stress factor is a very rough estimate. Generally used activity factors are: Postoperative, no infection 1.10, Major trauma 1.25, Trauma plus infection 1.50, Major burn 2.00. The stress factor is the most inaccurate part of the whole calculation. If serious hypermetabolism is present, it is always best to measure the energy expenditure. For the patient presented, the calculation of TEE is: TEE = BEE * 1.15 * 1.5.

A critically ill 60-year-old man, who has intra-abdominal infection following major liver injury, is being evaluated for intensive nutritional support. He is awake and oriented, breathing on his own, and confined to bed. He has fever spikes to 102°F every night. The basal energy expenditure (BEE) as calculated by the Harris-Benedict equation is 1600 kcal/24 hours. What is the best estimate of his caloric needs? A. 1600 B. 3840 C. 2040 D. 2760 E. 1840

B. systolic blood pressure and pulse The traditional techniques to monitor therapy for shock focus on changes in blood pressure, heart rate, and urine output. These conventional vital signs are convenient but not specific enough to guide resuscitation because they are affected by the patient's physiologic compensatory reserves. Multiple studies have shown that variables indicative of tissue perfusion correlate better with patient survival than do the more traditional central hemodynamic variables of blood pressure and heart rate. Significant improvement in survival is noted for patients who maintain a normal cardiac index and calculated oxygen delivery index during the first 24 hours after injury. Lactate levels are indicative of anaerobic tissue metabolism, which correlates with the severity of the shock state. There is a direct correlation between lactate and the more convenient measurements of arterial base deficit as expressed on the arterial blood gas determination. The central mixed venous oxyhemoglobin saturation is a sensitive parameter to gauge the degree of oxygen extraction by the peripheral circulation. Gastric mucosal pH is reflective of the adequacy of splanchnic perfusion.

A young, previously healthy patient involved in a jet-ski accident has a burst fracture of the liver. Palpable systolic pressure is 70 mm Hg. At celiotomy the area is packed after initial suture control of several large intraparenchymal liver vessels. The patient is taken to the intensive care unit for rewarming, correction of coagulopathy, and further resuscitation. The postoperative measured parameter that has the LEAST correlation with adequacy of resuscitation is: A. gastric mucosal pH B. systolic blood pressure and pulse C. blood gas base deficit D. central mixed venous oxyhemoglobin saturation E. serum lactate

C. a stocking or glove pattern Scalding injuries are common among abused children, and all physicians should be attuned to characteristics that may suggest an intentional injury. Most scalding injuries resulting from child abuse produce burn patterns indicating a more controlled and more prolonged exposure to a hot fluid than is likely to occur with unintentional scalding. The burned portion of the child's body frequently appears to have been "dipped" into the fluid that caused the injury, usually hot water. Thus, when an arm or leg has been injured in an abusive episode, the burn area will commonly be similar to the area of skin ordinarily covered by a glove or a stocking. Signs more likely to accompany unintentional scalding include irregular or blurred burn margins, burns likely to have been caused by splashing of the hot fluid, or a random distribution of the burn injury on the child's body. Unintentional scalding is also likely to be asymmetrical, if more than one extremity or the buttocks are involved.

Intentional scalding injuries in children are likely to be characterized by: A. asymmetry B. irregular or blurred margins C. a stocking or glove pattern D. random distribution E. splash marks

A. are usually administered through a tibial insertion site Intraosseous fluid infusions to replace blood volume loss are a standard part of the resuscitation for injured children. In the emergency setting, with less-than-optimal lighting, assistance, and choice of equipment, the intraosseous route does not require the precision demanded for cannulating the small vessels of children, yet provides a cannula large enough to deliver adequate volume. Although a number of osseous ports are feasible for this technique, the medial aspect of the tibia, 2 or 3 cm distal to the tibial tuberosity, is the usual site for insertion of the intraosseous needle. Colloid solutions, including blood, and crystalloids can be infused by this route. With maintenance of proper sterile procedures, infections associated with intraosseous punctures are not a problem. The intraosseous route has also been used in adults and may be the best option for adults who have no available peripheral veins when central vein cannulation or a cutdown is not an appropriate choice.

Intraosseous fluid infusions in children: A. are usually administered through a tibial insertion site B. are too cumbersome for use in emergencies C. are associated with osteomyelitis in about 5% of cases D. must be limited to crystalloids E. are contraindicated in children over age four

C. ipsilateral motor loss and contralateral sensory loss Associated with hemitransection of the spinal cord, this syndrome is characterized by unilateral damage to the corticospinal and spinothalamic tracts. This results in an ipsilateral motor defecit, and contralateral sensory defecits, specifically related to pain and temperature.

Traumatic injury of the lateral half of the spinal cord (Brown-Sequard syndrome) results in A. ipsilateral motor and sensory loss B. ipsilateral motor loss and no sensory loss C. ipsilateral motor loss and contralateral sensory loss D. ipsilateral sensory loss and contralateral motor loss E. contralateral motor and sensory loss

A. Enteral feedings should be started immediately on admission Until recently it was believed that the immense stress response initiated by severe burns produced a paralytic ileus that would preclude enteral feeding for several days postburn. More recent studies have shown that enteral feeding not only can be tolerated immediately after burning, but that paralytic ileus can actually be prevented. There is no need for gastric decompression if ileus is not present. The risk of aspiration with early feeding is minimal. Awake patients can protect their airway, and intubated patients usually have a cuffed endotracheal tube. In several studies the incidence of aspiration is about 3%—the same or less than the likelihood of intravascular sepsis from central venous catheters. H2 blockers have fallen into disfavor in preventing stress ulcers. Their effectiveness is no higher than sucralfate, and with H2 blockers the overall infection rate is several times higher.

Which of the following statements about using the gastrointestinal tract after burns larger than 30% of the total body surface area is TRUE? A. Enteral feedings should be started immediately on admission B. H2 receptor blockers are recommended for patients receiving continuous enteral feedings C. Because patients rarely tolerate feedings, total parenteral nutrition should be started D. Burn patients should not be allowed to take fluids by mouth because of the risk of aspiration E. The stomach should be decompressed using a nasogastric tube on low intermittent suction until resuscitation is complete

A. A Le Fort II fracture involves the nasal bones and may widen the inner canthi of the eyes The goal in complex facial trauma is to restore and maintain normal anatomy of the craniofacial skeleton. Definitive operative repair is initiated as soon as the patient is stabilized from a multitrauma standpoint prior to the onset of edema or deferred until the edema has cleared if the patients other injuries do not allow for immediate repair. A Le Fort I fracture is a horizontal maxillary fracture that will allow the maxillary arch to move in relation to the rest of the face. A Le Fort II fracture is a maxillary fracture that involves the nasal bone. A Le Fort III fracture results in craniofacial separation with the entire face moving in relation to the skull base. Le Fort III fracture involves the zygomatic arch, the superior lateral maxillary buttress, and the superior medial maxillary buttress.

Which of the following statements concerning Le Fort fractures is true? A. A Le Fort II fracture involves the nasal bones and may widen the inner canthi of the eyes B. A Le Fort I fracture divides the maxilla in half vertically C. Conservative treatment and antibiotic therapy are the mainstays in the management of Le Fort I fractures D. A Le Fort I fracture divides the mandible in half vertically E. A Le Fort III fracture divides the maxilla and nasal bones from the skull, but not the zygomatic compound