Anesthesia For Trauma And Burn Patients

Front 1

75% of mortality occurs in the hospital from trauma with in ____ hours

Back 1

48 hours,

Front 2

Possible contraindications to cricothyroidotomy

Back 2

include age younger than 12 years and suspected laryngeal trauma; permanent laryngeal damage may result in the former, and uncorrectable airway obstruction may occur in the latter situation.

Front 3

Induction agent contraindicated in brain and major vascular injuries?

Back 3

Ketamine due to increased ICP and BP, HR

Front 4

Indicators of spine injury in awake patients

Back 4

neck pain, tenderness, and extremity paresthesias

Front 5

C-spine clearance for awake patient

Back 5

(1) no midline cervical tenderness, (2) no focal neurologic deficit, (3) normally alert, (4) not intoxicated, and (5) no distracting painful injury

Front 6

The Canadian C-Spine Rule for Radiography after Trauma

Back 6

(1) Is there any high-risk factor mandating radiography? (2) Are there low-risk factors that permit safe evaluation of the range of motion of the neck? (3) Can the patient rotate the neck laterally for 45 degrees in each direction without pain? Comparison of these two sets of criteria showed that the Canadian Rule is more reliable than NEXUS in diagnosing cervical spine injury in responsive patients.

Front 7

The Eastern Association for the Surgery of Trauma (EAST) guidelines for radiographic clearance of c-spine for patients w/ risk factors for injury

Back 7

3 views AP, lateral and open mouth and head CT

Front 8

Stable fractures of the c-spine

Back 8

Stable fractures of the spine are spinous process fractures; isolated osteophyte, trabecular, transverse process, and avulsion fractures without ligament injury; and wedge compression fractures with loss of ≤25% of vertebral body heigh

Front 9

Standard measure of diganosing ligmentous injury

Back 9

flexion and extension series
however, MRI is more accurate

Front 10

Nasothracheal intubation risks in trauma patients

Back 10

epistaxis, failure of intubation, and the possibility of entry of the endotracheal tube into the cranial vault or the orbit if there is damage to the cranial base or the maxillofacial complex.

Front 11

increased possibility of cranial injury w/ the following

Back 11

midface fractures involving the frontal sinus, as well as the orbitozygomatic and orbitoethmoid complexes.

Front 12

Clinical signs of penetrating cervical airway trauma

Back 12

escape of air, hemoptysis, and coughing are present in almost all patients

Front 13

major blunt laryngotracheal damage signs on presentation

Back 13

includes hoarseness, muffled voice, dyspnea, stridor, dysphagia, odynophagia, cervical pain and tenderness, ecchymosis, subcutaneous emphysema, and flattening of the thyroid cartilage protuberance (Adam's apple).

Front 14

blunt laryngeal trauma patients may also have which condition?

Back 14

cervical spine injury, in 70%
no cricothroidotomy or blind intubation!

Front 15

signs of thoracic airway injuries

Back 15

Pneumothorax, pneumomediastinum, pneumopericardium, subcutaneous emphysema, and a continuous air leak from the chest tube are the usual signs of this injury; they occur frequently but are not specific for thoracic airway damage. In patients intubated without the suspicion of a tracheal injury, difficulty in obtaining a seal around the endotracheal tube or the presence on a chest radiograph of a large radiolucent area in the trachea corresponding to the cuff suggests a perforated airway.

Front 16

Complications of thoracic airway injury repair

Back 16

suboptimal and complicated by stump leak and empyema, suture line stenosis, or the need for tracheostomy or pneumonectomy.

Front 17

Which patients should be managed surgically for thoracic airway injury

Back 17

Patients with lesions larger than 4 cm, cartilaginous rather than membranous injuries, concomitant esophageal trauma, progressive subcutaneous emphysema, severe dyspnea requiring intubation and ventilation, difficulty with mechanical ventilation, pneumothorax with an air leak through the chest drains, and/or mediastinitis are still managed surgically. Those without these problems may be treated nonoperatively with a reasonable outcome.

Front 18

Signs of flail chest

Back 18

Coexisting hemopneumothorax, paradoxical chest wall movement, and/or pain-induced splinting, history of trauma

Front 19

what is predictive of development of ARDS in patient w/ flail chest?

Back 19

once the contusion volume exceeds 20% of total lung volume

Front 20

Management of flail chest w/o gas abnormalities

Back 20

conservative - epidural analgesia w/ local and opioids, no need for resp support until pt can't exchange gasses, otherwise increase in morbidity and mortality.

Front 21

which patient's should get intubated for flail chest

Back 21

pulmonary contusion, respiratory insufficiency, or failure despite adequate analgesia, clinical evidence of severe shock, associated severe head injury, or injury requiring surgery, airway obstruction, and significant pre-existing chronic pulmonary disease

Front 22

Ventilation settings for trauma patients

Back 22

. Positive end-expiratory pressure (PEEP) with low tidal volumes (6 to 8 mL/kg) and low inspiratory alveolar or plateau pressures should be used to decrease the likelihood of ARDS if ventilation is controlled

Front 23

ventilation settings in severe bilateral pulmonary contusion patients

Back 23

differential lung ventilation via a double-lumen endobronchial tube, or high-frequency jet ventilation may enhance oxygenation and cardiac function, which may be compromised by concomitant myocardial contusion or ischemia

Front 24

Base deficit in shock for mild, mod and severe trauma.

Back 24

A base deficit between 2 and 5 mmol/L suggests mild shock, between 6 and 14 mmol/L indicates moderate shock, whereas >14 mmol/L is a sign of severe shock. An admission base deficit in excess of 5 to 8 mmol/L correlates with increased mortality

Front 25

Class I trauma
blood loss
HR
BP
RR
Urine output
mental status
fluid replacement

Back 25

<750 ml
<15%
<100 HR
normal BP
14-20 RR
> 30 ml urine
Slightly anxious
crystaloid

Front 26

Class II trauma
blood loss
HR
BP
RR
Urine output
mental status
fluid replacement

Back 26

750-1500
15-30 %
>100 HR
normal BP
20-30 RR
urine output of 20-30 ml/hr
mildly anxious
crystaloid

Front 27

Class III trauma
blood loss
HR
BP
RR
Urine output
mental status
fluid replacement

Back 27

1500-2000
30-40%
>120 HR
decreased BP
30-40 RR
urine 5-15
anxious and confused
crystaolloid + blood

Front 28

Class IV trauma
blood loss
HR
BP
RR
Urine output
mental status
fluid replacement

Back 28

> 2L blood
> 40 %
> 140 HR
Decreased BP
> 35 RR
urine output negligible
confused and lethargic
crystalloid + blood

Front 29

transfusion threshold in trauma

Back 29

hematocrit <25% for young, healthy patients and <30% for older patients or those with coronary or cerebrovascular disease

Front 30

vicious cycle or lethal triad of trauma

Back 30

acidosis, hypothermia and coagulopathy

Front 31

fluid therapy for severe trauma

Back 31

liquid plasma replacement along with fluids and PRBCs as soon as the patient arrives in the emergency department, and continuing it throughout surgery.

Front 32

what is liquid plasma and how does it differ from FFP

Back 32

Liquid plasma differs from fresh-frozen plasma (FFP) in that it is frozen at -180°C within 8 to 24 hours, whereas FFP is frozen within 8 hours. It contains all of the stable proteins found in FFP, although in slightly lower concentrations. The major difference is a 25% reduction of factor VIII. One unit of FFP contains approximately 7% of the coagulation factor activity of a 70-kg man.

Front 33

most important cause of death in head-injury patients?

Back 33

hypotension
a single episode of systolic blood pressure <90 mm Hg is associated with a 50% increase in mortality, and subsequent episodes or lower pressures78 increase mortality even further.

Front 34

most appropriate thearpeutic interventions for head trauma

Back 34

normalization of the systemic blood pressure (mean blood pressure >80) and maintaining the Pao2 >95, the ICP <20 to 25 mm Hg, and the CPP 50 to 70 mm Hg. 30 degrees head elevation, sedation and neuromuscular blockers are given as necessary, and cerebrospinal fluid is drained through a ventriculostomy catheter, if available. Rapid and adequate restoration of the intravascular volume with isotonic crystalloid and, if necessary, with colloid solutions should be aimed at maintaining the CPP between 50 and 70 mm Hg while attempting to minimize further brain swelling.

Front 35

crystaloid of choice for brain trauma

Back 35

NS, since LR is slightly hypotonic

Front 36

diuretic of choice for head trauma

Back 36

mannitol

Front 37

mannitol toxicity and adverse effects

Back 37

hyponatremia, high serum osmolality, and a gap between calculated and measured serum osmolality >10 mOsm/L, may result when the drug is given in large doses (2 to 3 g/kg) or to patients with renal failure. Mannitol should be used with great care in the presence of hypotension, sepsis, nephrotoxic drugs, or pre-existing renal disease as these may also precipitate renal failure. the effects of mannitol result from its activity in regions of the brain where the blood–brain barrier is intact. It may exacerbate edema in injured areas in which it may easily enter the tissues.

Front 38

what is AVDo2

Back 38

1.34 · Hgb · (Sao2 – Sjvo2), with the saturations expressed as decimal values, and normally is approximately 6. An increase in this value is a sign of insufficient blood flow, whereas a subnormal level indicates hyperemia. A reduction in ICP with elevation of CPP during treatment is reflected by a rise in Sjvo2 and a narrowing of the AVDo2, presumably reflecting an improvement in the circulation to the brain.

Front 39

criticism of use of AVDO2 in brain injured patient

Back 39

reflects global 02 consumption, not in the ischemic area

Front 40

when one should use barbiturates to decrease ICP in head injured patients?

Back 40

only for refractory high ICP

Front 41

predictors of spine injury

Back 41

a history of a motor vehicle, industrial, or athletic accident, an act of violence, or a fall; penetrating trauma resulting in a neurologic deficit below a specific spinal level; or pain and tenderness over the involved vertebrae

Front 42

does spinal pain always localize to the level of injury?

Back 42

No

Front 43

signs of spinal injury in comatose patients

Back 43

flaccid areflexia, loss of rectal sphincter tone, paradoxical respiration, and bradycardia in a hypovolemic patient suggest the diagnosis

Front 44

harmful side-effects of steroid therapy for spinal cord patients

Back 44

increased rate of sepsis, pneumonia, and days of intensive care and positive-pressure ventilation, and is also associated with increased mortality in the 36 to 74% of patients with spine injuries who also have head injuries

Front 45

at which C-spine level will a patient need ventilatory assistance?

Back 45

C 4 and above

Front 46

neuromuscular blockade in quadriplegic patients

Back 46

avoid succinylcholine , may use Roc to intubate if RSI is desired

Front 47

indication for thoracotomy in patients w/ hemothorax

Back 47

Initial drainage of 1,000 mL of blood, or collection of >200 mL/hr for several hours, a “white lung” appearance on the anteroposterior chest radiograph, or a continuous major air leak from the chest tube

Front 48

What is VATS? when does it need to be performed?

Back 48

Hemodynamically stable patients with persistent bleeding of <150 mL/hr are managed with video-assisted thoracoscopic surgery (VATS) to control bleeding. This procedure requires placement of a double-lumen tube to collapse the lung on the involved side; it can also be useful in diagnosis of suspected diaphragmatic, cardiac, or mediastinal injuries; evaluation of some bronchopleural fistulas; and evacuation of clotted blood or an empyema that does not drain with a chest tube. Use of VATS decreases the need for open thoracotomy and the number of negative explorations in stable trauma patients

Front 49

consequences of penetrating cardiac trauma?

Back 49

Pericardial tamponade, cardiac chamber perforation, and fistula formation between the cardiac chambers and the great vessels

Front 50

classic findings of cardiac tamponade?

Back 50

tachycardia, hypotension, distant heart sounds, distended neck veins, pulsus paradoxus, or pulsus alternans

Front 51

findings in cardiac injury? after blunt trauma

Back 51

angina, sometimes responding to nitroglycerin, dyspnea, chest wall ecchymosis and/or fractures; dysrhythmias of any type; and right-sided or left-sided congestive heart failurea

Front 52

diagnosis of cardiac injury? after blunt trauma

Back 52

The diagnosis is based on the 12-lead ECG, troponin I level, and echocardiography. The ECG is very sensitive, although not specific. A normal trace cannot rule out the diagnosis, but it is the best screening test. Common ECG abnormalities include almost any type of dysrhythmia, ST or T-wave changes, and conduction delays.

Front 53

Clinical sings of aortic injury?

Back 53

Increased arterial pressure and pulse amplitude in upper extremities
Decreased arterial pressure and pulse amplitude in lower extremities
Absent or weak left radial artery pulse
Osler's sign: discrepancy between left and right arm blood pressure
Retrosternal or interscapular pain
Hoarseness
Systolic flow murmur over the precordium or medial to the left scapula
Neurologic deficits in the lower extremities

Front 54

radiographic features of aortic injury?

Back 54

Widened mediastinum
Blurring of the aortic contours
Widened paraspinal interfaces
Left apical cap
Opacified aortopulmonary window
Broadened paratracheal stripe
Displacement of the left main-stem bronchus
Displaced SVC
Rightward deviation of the esophagus and trachea
Nasogastric tube shift
Left hemothorax
Sternal and/or upper rib fractures
Lung contusion
Pneumothorax

Front 55

ct findings in aortic injury

Back 55

Mediastinal hematoma
Aortic wall irregularity
Intimal flap
False aneurysm
Pseudocoarctation
Intramural hematoma
Intraluminal clot or medial flap

Front 56

ultrasound findings for aortic injury

Back 56

Intimal flap
Turbulent flow
Dilated aortic isthmus
Acute false aneurysm
Intraluminal medial flap
Hemothorax
Hemomediastinum

Front 57

at which anatomical point does thoracic aortic injury mostlikely appear?

Back 57

at the isthmus—the junction between the free and fixed portions of the descending aorta—in 90% of cases, and carries an 80% mortality in the first hour following injury.

Front 58

classification of thoracic aortic injuries with TEE?

Back 58

grade 1 injury consists of an intramural hematoma, limited intimal flap and/or mural thrombus; grade 2 injury consists of subadventitial rupture, injury to the media, altered aortic geometry and/or small hemomediastinum; grade 3 injury consists of transsection with massive blood extravasation, intraluminal obstruction causing pseudocoarctation, and ischemia

Front 59

which class based on TEE for thoracic aortic injuries could be treated w/ observation?

Back 59

class 1: intramural hematoma, limited intimal flap and/or mural thrombus

Front 60

Pelvic fractures, management of bleeding

Back 60

external fixation and extraperitoneal packing of the pelvis in the OR followed by angiography and possible embolization is more beneficial than only external fixation and angiography

Front 61

Delayed fracture repair is associated with?

Back 61

an increased risk of deep vein thrombosis (DVT), pneumonia, sepsis, and the pulmonary and cerebral complications of fat embolism. In open fractures, an additional important concern is infection. Wounds left unrepaired for more than 6 hours are likely to become septic.

Front 62

sings of vascular trauma in patients w/ extremity fractures

Back 62

pain, pulselessness, pallor, paresthesias, and paresis

Front 63

Indication for surgery in patients w/ compartment syndrome?

Back 63

A pressure exceeding 40 cm H2O is an indication for immediate surgery.

Front 64

partial-thickness burn

Back 64

is red, blanches to touch, and is sensitive to painful stimuli and heat.

Front 65

Superficial burns ( first degree) involve the :
and heal?

Back 65

burns involve the epidermis and upper dermis, and heal spontaneously

Front 66

Deep partial-thickness (second-degree) involve?
and how are they managed?

Back 66

deep dermis and require excision and grafting to ensure rapid return of function

Front 67

Deep burns ( third degree), what does it look like?
management?

Back 67

does not blanch even with deep pressure and is insensate
Complete destruction of the dermis requires wound excision and grafting to prevent wound infection that may lead to local sepsis and systemic inflammation

Front 68

Fourth degree burns involve....
management?

Back 68

involve muscle, fascia, and bone, necessitating complete excision and leaving the patient with limited function.

Front 69

systemic effects of a severe burn

Back 69

stimulates the release of mediators such as interleukins, tumor necrosis factor, and neopterins, locally—producing wound edema—and into the circulation, resulting in immune suppression, hypermetabolism, protein catabolism, sepsis, and multisystem organ failure. Burns >40% TBSA consistently develop catabolism and weight loss that may last up to 1 year

Front 70

which pharmacological agents can decrases the catabolism in severe burns?

Back 70

low-dose insulin infusion, beta-blockade, and the synthetic testosterone analogue oxandrolone

Front 71

following a burn, how long does it take to develop parenchymal lung injury?

Back 71

1-5 days to ARDS

Front 72

Late lung complications of burns?

Back 72

pneumonia and PE, take longer than 5 days to develop

Front 73

ventialtory support in intubated burn patients?

Back 73

low levels of PEEP will prevent the pulmonary edema that may develop secondary to loss of laryngeal auto-PEEP in patients with significant airway obstruction before intubation. Airway humidification, bronchial toilet, and bronchodilators if needed for bronchospasm are also indicated.

Front 74

how does CO poisoning cause tissue hypoxia

Back 74

by its 200-fold greater affinity for hemoglobin than oxygen and by its ability to shift the hemoglobin dissociation curve to the left, impairing O2 unloading to the tissues. It also interferes with mitochondrial function, uncoupling oxidative phosphorylation and reducing adenosine triphosphate production, thus causing metabolic acidosis. CO can be a direct myocardial toxin, preventing survival in patients who suffer cardiac arrest

Front 75

does normal pulse ox reading exclude CO poisoning?

Back 75

No, although arterial gas w/ co-oxymeter does

Front 76

at which CO concentration does blood turn cherry-red?

Back 76

> 40%

Front 77

List symptoms for the following COHbc level?
< 15-20
20-40
40-60
>60

Back 77

1. headache, dizziness, and occas confusion
2. nausea, vomiting, disorientation, visual impairment
3. agitation, combativeness, hallucinations, coma, shock
4. death

Front 78

at which COHb level is hyperbaric oxygen recommended

Back 78

> 30 %

Front 79

Other cause of hypoxia in burned patients than CO toxicity?

Back 79

Cyanide toxicity

Front 80

cyanide toxicity presentation

Back 80

unexplained metabolic acidosis, neuro symptoms, agitation, confusion, coma, elevated plasma lactate

Front 81

what is the toxic level of cyanide?

Back 81

0.2 mg/L and lethal leve is above 1 mg/ L

Front 82

management of cyanide toxicity victim?

Back 82

oxygen at high flows. the ion has short half life and pharmacological therapies - thiosulfate, amyl nitrate, sodium nitrate- offer no additional benefit.