Search our site 
 
Advanced Search
 
Home | Exam dates | Contact us | About us | Testimonials |
 
 

map

UBP Question 1

 border=Email this page
 



Question 1

 

(Short Form)



A 5’7’’, 180 kg, 22-year-old male is brought to the trauma suite following a motor vehicle accident. He is somnolent, uncooperative, spontaneously breathing, withdraws from painful stimuli (does not localize), and is speaking inappropriately. On examination, he has a swollen right leg, ecchymosis into the periorbital tissue, hemotympanum, multiple facial fractures, and multiple loose teeth. There is an 18g IV in his left arm with D5LR hanging. Vital Signs: P = 134, R = 24, BP = 178/108, O2 sat = 96% on non-rebreathing mask, T = 33 °C

Pre-operative Management


1) What is the Glasgow Coma Scale?

2) The patient opens his eyes to pain. What is his score?

3) What are your treatment goals in this patient?

4) Would you intubate this patient?

5) The patient is becoming more combative. How will you intubate him?

6) Are you comfortable using Succinylcholine?

7) The neck radiographs show no apparent injury. Is this patient’s C-spine clear?

8) What are the criteria to clear a C-spine?

9) You are having difficulty placing the endotracheal tube with direct laryngoscopy, and the resident suggests a blind nasal technique. How would you respond?

10) Ok, the patient is intubated. What do you make of his initial vital signs?

11) Does this patient require fluid resuscitation?

12) Are you ok with the D5LR that is currently hanging? Any concerns with LR?

13) Would you lower the blood pressure?

14) What is the equation for cerebral perfusion pressure?

15) Isn’t there autoregulation of blood flow to the brain? What is the range for normal cerebral autoregulation?

16) What is normal CPP? What is ideal in a patient with traumatic head injury?

Pre-operative Management

1) What is the Glasgow Coma Scale?

UBP Answer: A scoring system based on eye opening, best motor response, and best verbal response that has a strong correlation with severity of head injury and patient outcome. A score of 8 or less which persists for 6 hours is considered severe injury and is associated with a mortality rate of approximately 35%. A score of 9-12 suggests moderate injury and a score of 13-15 suggests mild injury.

2) The patient opens his eyes to pain. What is his score?

UBP Answer: Given that he opens his eyes with painful stimuli (2), withdraws from pain (4), and is exhibiting inappropriate speech (3), his score would be a 9, suggesting moderate brain injury.


Glasgow Coma Scale:

 

 

 

 

Patient Response

Score

 

 

 

Eye Opening

Spontaneous

4

 

To Speech

3

 

To Pain

2

 

None

1

 

 

 

Verbal Response

Oriented

5

 

Confused Speech

4

 

Inappropriate Speech

3

 

Incomprehensible Sounds

2

 

None

1

 

 

 

Best Motor Response

Obeys Commands

6

 

Localizes Pain

5

 

Withdraws to Pain

4

 

Decorticate Flexion

3

 

Decerebrate Extension

2

 

No Response

1

 

 

 



3) What are your treatment goals in this patient?

UBP Answer: My initial goals are to assess and secure his airway and then achieve hemodynamic stabilization. Additionally, I would treat and avoid contributory factors to secondary neurologic injury such as hypoxia, hypercarbia, hypotension, and anemia. Finally, a full body assessment for injuries would be performed if not done simultaneously.

4) Would you intubate this patient?

UBP Answer: Given the potential difficulty of managing his airway due to his super morbid obesity, facial injuries, C-collar, and signs consistent with basilar skull fracture, I would be very concerned that further deterioration of his mental status could place me in the position of managing his airway emergently (i.e. apnea). Moreover, this patient with a significant head injury may not tolerate the hypercapnia-induced increases in cerebral blood flow, and subsequent increase in ICP, associated with hypoventilation or apnea. Therefore, I would proceed with intubation, despite the presence of spontaneous ventilation, to reduce the risk of aspiration, hypoventilation, apnea, and to forego the necessity of managing his difficult airway under more emergent conditions.

5) The patient is becoming more combative. How will you intubate him?

UBP Answer: My primary goal is to safely secure the potentially difficult airway of this uncooperative and super morbidly obese patient who has facial injuries, a C-collar in place, and signs consistent with a basilar skull fracture (which would eliminate nasal intubation as an acceptable alternative). However, while intubating him I would attempt to avoid: (1) factors that may contribute to increased intracranial pressure, such as hypoxia, hypercarbia, and sympathetic stimulation; (2) hypotension, which may lead to inadequate end-organ perfusion (cerebral perfusion is particularly at risk if his intracranial pressure is elevated); (3) cervical spine injury; and (4) aspiration of either gastric contents or damaged teeth. Therefore, since an awake fiberoptic intubation would not likely prove successful (uncooperative, facial/airway trauma), I would (1) ensure the availability of difficult airway equipment; (2) have the surgeon at bedside and ready to perform a tracheostomy, if necessary; (3) place the patient in 30° reverse-trendelenburg to improve respiratory mechanics, facilitate intubation, and reduce the risk of passive regurgitation (make sure that this positioning is hemodynamically tolerated); (4) pre-oxygenate the patient; (5) carefully titrate intravenous ketamine, in an attempt to achieve an adequate plane of anesthesia while maintaining spontaneous respiration; (6) remove the front of the cervical collar to allow for the application of cricoid pressure; (7) ensure in-line manual stabilization; and (8) perform careful laryngoscopy for ETT placement.

6) Assuming you are concerned about elevated intracranial pressures, is it advisable to utilize ketamine for induction?

UBP Answer: Ketamine-induced increases in sympathetic tone, cerebral blood flow (may increase 50-60% secondary to cerebral vasodilation), and regional CMRO2 (total CMRO2 is not increased because increases in some areas of the brain are balanced by decreases in other areas) are undesirable in this patient with potentially elevated ICP. However, my overriding goal when inducing this patient with a potentially difficult airway is to maintain spontaneous respirations throughout induction and intubation. Therefore, given the minimal effects of carefully titrated ketamine on ventilatory drive, I would administer this drug for induction, recognizing that the potential detrimental effects on ICP are small in comparison to those associated with hypoxia, hypercarbia, and loss of the airway.

7) Shouldn’t you use succinylcholine for ETT placement?

UBP Answer: While succinylcholine would be desirable in optimizing intubating conditions and reducing the risk of aspiration, I would not utilize it in this case due to concerns for difficult airway management and potentially elevated ICP. My primary reason for avoiding succinylcholine is the risk of inducing apnea in this patient with potentially elevated ICP (hypoxia and/or hypercarbia lead to increased ICP) and several risk factors for difficult airway management (i.e. super morbid obesity, facial fractures, loose teeth, lack of cooperation, and a C-collar). Moreover, the transient increase in ICP associated with succinylcholine (possibly secondary to fasciculations) would be undesirable in this patient with apparent head trauma (although this succinylcholine-induced increase in ICP tends to be transient and small in comparison to that which would result from hypoxia or hypercarbia).

8) The neck radiographs show no apparent injury. Is this patient’s C-spine clear?

UBP Answer: It is impossible to clear this patient’s C-spine given his mental status, which makes it impossible to rule out pain upon palpation of the cervical spine. Radiographs should include anterior/posterior, odontoid, and lateral neck views showing C1 through T1. Despite all of these radiographs showing no injury, 7% of fractures are still missed and ligamentous injury is not ruled out.

9) What are the criteria to clear a C-spine?

UBP Answer: The criteria include: 1) no cervical pain or tenderness, 2) no paresthesias or neurologic deficits, 3) normal mental status, 4) no distracting pain, and 5) >4 years of age. If the above criteria are not met then a negative lateral c-spine showing C1 through T1; an open mouth odontoid view; and thoracolumbar, anterior/posterior, and lateral plain films should be obtained.

10) You are having difficulty placing the endotracheal tube with direct laryngoscopy, and the resident suggests a blind nasal technique. How would you respond?

UBP Answer: Given the presence of periorbital ecchymosis and hemotympanum, it would be inappropriate to perform a blind nasal intubation as these findings suggest a possible basilar skull fracture. With this type of fracture, there is a risk of advancing the ETT into the brain when attempting a blind nasal intubation.
11) Ok, the patient is intubated. What do you make of his initial vital signs?

UBP Answer: A hyperdynamic circulatory response is not unusual following head injury and may result from a surge in epinephrine. Additionally, pain, hypoxia, hypercarbia, hypovolemia, and/or anemia could be responsible for his tachycardia and hypertension. In either case, I would attempt to optimize the patient by controlling his pain, replacing fluid losses with blood products or crystalloid as necessary, and ensuring adequate ventilation. Given my concerns about potentially elevated ICP and decreased cerebral perfusion pressure, I would probably avoid treating his tachycardia and hypertension with a ß-blocker or vasodilator. If treatment of this kind was deemed necessary, I would use a short acting agent like esmolol. This patient is also mildly hypothermic which may be beneficial in so far as it reduces CMRO2.

12) Does this patient require fluid resuscitation?

UBP Answer: Possibly. I would perform a thorough exam with special attention to urine output (if a Foley catheter is in place), mucous membranes, cap refill, and blood loss, recognizing that there could be hidden blood loss in the abdominal compartment or secondary to the right femur fracture. My goals in fluid resuscitation are to maintain cerebral perfusion pressure by restoring circulating blood volume and avoiding hypotension. At the same time, I want to reduce the risk of cerebral edema by maintaining serum osmolality and avoiding significant reductions in colloid oncotic pressure.

13) Are you ok with the D5LR that is currently hanging? Any concerns with LR?

UBP Answer: I do have a problem with the D5LR since hyperglycemia may augment ischemic brain injury. For this reason, glucose containing solutions are usually avoided in patients with brain injury. Theoretically, the small amount of free water in lactated Ringer’s solution (100 mL of free water per liter) could result in increased brain edema as compared to an isotonic solution such as normal saline.

14) Would you lower the patient’s blood pressure if it increased to 205/118 mmHg?

UBP Answer: This blood pressure is very high and would require treatment. If it remained elevated after ensuring adequate analgesia, intravascular volume replacement, and adequate ventilation, I would administer a short acting agent, such as esmolol, to lower his blood pressure to a safe level. However, I would not attempt to normalize his blood pressure since higher than normal blood pressures may be necessary to provide adequate cerebral perfusion in the presence of elevated ICP (CPP = MAP – ICP). Also, since the patient’s injury and mental status suggest the strong possibility of elevated ICP, I would take steps to reduce his intracranial pressure in an effort to reduce the risk of inducing cerebral ischemia with treatment of his blood pressure. I would also discuss with the surgeon the potential benefits of placing an ICP monitor to aid in fluid resuscitation and monitoring of ICP.


15) What is the equation for cerebral perfusion pressure?

UBP Answer: MAP – ICP or CVP (whichever is greater).

16) Isn’t there autoregulation of blood flow to the brain? What is the range for normal cerebral autoregulation?

UBP Answer: While autoregulation may be intact, it is quite possible that this regulatory mechanism is abolished in the presence of head trauma, making cerebral blood flow pressure dependent. In the absence of chronic hypertension, intact cerebral autoregulation maintains cerebral blood flow at a constant rate with mean arterial pressure ranging from 60 – 150 mmHg.

17) What is normal CPP? What is ideal in a patient with traumatic head injury?

UBP Answer: Normal CPP is around 80 – 100 mmHg. In a patient with head injury the optimum CPP is unknown. While earlier studies suggested improved outcomes with a CPP of 70 -80 mmHg, three recent studies have shown that CPP > 70 mmHg may increase the incidence of ARDS. Additionally, some studies indicate that cerebral ischemia may occur in the head injury patient with CPP below 50 – 60 mmHg. Therefore, it would seem reasonable to try to maintain a CPP of 60 – 70 mmHg (Note: some sources state a goal of 50-60 mmHg).


(Long Form)


A 5’7’’, 180 kg, 22-year-old male is brought to the trauma suite following a motor vehicle accident. He is somnolent, spontaneously breathing, withdraws from painful stimuli (does not localize), and is speaking inappropriately. The patient has an 18g IV in his left arm with D5LR hanging.


PE: VS: P = 134, R = 24, BP = 178/108, O2 sat = 96% on non-rebreathing mask, T = 33 °C

HEENT: There is an abrasion on the forehead. There is ecchymosis into the periorbital tissue and hemotympanum is noted. The patient has a C-collar in place.

Airway: There are multiple facial fractures, multiple loose teeth, and the patient is uncooperative for further examination.

Lower Extremities: The right leg is swollen with intact peripheral pulses.

Lab Hgb = 13.6, Hct = 42%, Platelets = 163,000.
Electrolytes: normal.

CT scans of the abdomen and pelvis: negative

CT scan of the head shows a non-displaced basilar skull fracture

Radiographs show a right femoral fracture. Neck radiographs show no apparent injury.

EKG: sinus tachycardia

Drug screen: positive for amphetamines



Intra-operative Management

1) Let’s assume there is an open femur fracture and the orthopedic surgeon wants to go straight to the OR. Would you require ICP monitoring in this patient?

2) What can you do to reduce increased ICP in the absence of an intraventricular catheter?

3) So, would you ever hyperventilate a patient with head trauma? What is the problem with hyperventilation?

4) The patient’s temperature is 33 C°. Does this concern you?

5) Would you use N2O on a patient with traumatic brain injury (TBI) and elevated ICP?

6) During the case the patient’s blood pressure progressively falls to 95/60 mmHg and peak inspiratory pressures increase to the mid 40’s. His oxygen saturation falls to the high 80’s. What is your differential? What are you going to do?

7) A pulmonary artery catheter is inserted and shows a PA pressure of 55/47 mmHg, a PCWP of 16 mmHg, a mixed venous oxygen saturation of 65%, and a cardiac index is 1.7 L/min/m2. Furthermore, on examination of the patient, you discover subconjunctival petechiae. How do you interpret this data?

8) Assuming this is fat emboli syndrome (FES), what would you do?


Post-operative Management

1) The following day the PaO2 is 88 mmHg with a FiO2 of 50% and the CXR shows bilateral diffuse infiltrates. What do you think might be going on?

2) What is required for the diagnosis of ARDS?

3) What is the recommended treatment?

4) The surgery resident recommends steroids, PEEP, and 10 ml/kg tidal volume. What do you think of this recommendation?

5) On post-op day 5 the patient’s serum sodium is 129 mEq/L and the urinary sodium is 105 mEq/L. What do you think might be going on?

6) How can you tell the difference between CSWS and SIADH?

7) Is it important to distinguish between the two?

Intra-operative Management


1) Let’s assume there is an open femur fracture and the orthopedic surgeon wants to go straight to the OR. Would you require ICP monitoring in this patient?

UBP Answer: I would not necessarily require ICP monitoring, but I would certainly discuss it with the surgeon, as the monitor may be very helpful in determining the mean arterial pressure required for adequate CPP. Moreover, the placement of an intraventricular catheter would, in addition to providing a means for monitoring ICP, allow for the removal of CSF should it become necessary to lower ICP and improve cerebral perfusion.

2) What can you do to reduce increased ICP in the absence of an intraventricular catheter?

UBP Answer: There are several actions I can take to decrease ICP including: (1) making sure there is no venous obstruction, particularly in this patient with a c-collar in place; (2) elevating the patient’s head 15-30 degrees (if hemodynamically tolerated) to increase venous drainage; (3) administering mannitol, which reduces ICP by osmotically shifting fluid from the brain compartment to the intravascular compartment, decreasing production of CSF (this affect is seen with hypertonic fluids), and inducing reflex cerebral vasoconstriction secondary to decreased blood viscosity (keep in mind that this drug may potentially worsen cerebral edema if the BBB is not intact, and/or result in the expansion of an intracranial hematoma as surrounding brain tissue shrinks with osmotic diuresis); (4) administering furosemide, recognizing that in the presence of hypovolemia, this diuretic could lead to hypotension and worsening cerebral ischemia; and (5) administering a barbiturate, which produces a beneficial effect by reducing ICP (secondary to cerebral vasoconstriction) and CMRO2 (although not globally), recognizing that there is a risk for hypotension when utilizing the large doses required for cerebral protection. While hyperventilation would reduce his ICP by inducing cerebral vasoconstriction, this is no longer recommended in head trauma patients due to the risk of inducing cerebral ischemia (patients with head trauma often experience a reduction in cerebral blood flow during the first 24 hours following the injury).

3) So, would you ever hyperventilate a patient with head trauma? What is the problem with hyperventilation?

UBP Answer: I would consider hyperventilation to a CO2 of 25-30 mmHg if other methods to reduce ICP were unsuccessful and I thought the elevated ICP was severe enough to place the patient at risk for brain stem herniation. However, as mentioned before, there is a risk of exacerbating cerebral ischemia by inducing cerebral vasoconstriction in a patient with lower than normal cerebral blood flow following head trauma. I would also keep in mind that the effects of hyperventilation are temporary (24-48 hours) because HCO3 levels in the CSF adjust to compensate for the change in PaCO2.

4) The patient’s temperature is 33 C°. Does this concern you?

UBP Answer: This does concern me because hypothermia has several deleterious effects including coagulopathy, cardiac dysrhythmias, impaired renal function, and poor wound healing. Additionally, although the reduction of CMRO2 by 7%/C° below 36 C° could theoretically provide some neuroprotection, the evidence has not shown improved neurologic outcome with mild hypothermia following traumatic brain injury.

5) Would you use N2O on a patient with traumatic brain injury (TBI) and elevated ICP?

UBP Answer: I would avoid the use of N2O for a patient with elevated ICP for several reasons. First, if cerebral perfusion were compromised, I would want the patient breathing 100% Oxygen. Second, if hyperemia was a problem, N2O has the potential to increase CBF when used alone or in conjunction with another volatile agent. Finally, if there were air trapped within the cranium, N2O would expand the air pocket, further elevating ICP.

6) During the case the patient’s blood pressure progressively falls to 95/60 mmHg and peak inspiratory pressures increase to the mid 40’s. His oxygen saturation falls to the high 80’s. What is your differential? What are you going to do?

UBP Answer: My differential would include migration of the ETT into the right mainstem, an unrecognized and expanding tension pneumothorax, cardiac tamponade, and fat emboli secondary to the patient’s fractured femur. I would hand ventilate, auscultate the chest, make sure the patient was breathing 100% O2, verify correct positioning of the ETT, and order a CXR. I may order an ABG, place a pulmonary catheter, and/or order an echocardiogram if the clinical picture is confusing.

7) A pulmonary artery catheter is inserted and shows a PA pressure of 55/47 mmHg, a PCWP of 16 mmHg, a mixed venous oxygen saturation of 65%, and a cardiac index is 1.7 L/min/m2. Furthermore, on examination of the patient, you discover subconjunctival petechiae. How do you interpret this data?

UBP Answer: The combination of hypoxia, elevated pulmonary artery pressure, decreased cardiac index, and subconjunctival petechiae in a patient with a long bone fracture, is most consistent with fat embolism syndrome. A definitive diagnosis, however, would require at least one major criterion and four minor criteria, as described by Gurd and Wilson*. Major criteria include: (1) a petechial rash, present on the conjunctiva, oral mucosa, axillae, and/or the skin folds of the neck; (2) hypoxemia, with a PaO2 < 60 mmHg on a FiO2 < 0.4; (3) central nervous system depression, unexplained by the patient’s hypoxia; and (4) pulmonary edema. Minor criteria include: (1) tachycardia, > 110 beats/minute; (2) pyrexia; (3) retinal fat emboli; (4) fat microglobulinemia; (5) fat globules in the sputum; (6) unexplained anemia; (7) unexplained thrombocytopenia; (8) increased erythrocyte sedimentation rate; (9) urinary fat globules; and (10) jaundice.

Recognizing that many of these diagnostic criteria would be confounded by conditions associated with his recent trauma, (i.e. pain ? tachycardia; hypovolemia ? tachycardia; head injury ? central nervous system depression; bleeding ? anemia and thrombocytopenia; etc.), I would attempt to obtain a more definitive diagnosis by evaluating the patient’s temperature, ABGs, CXR, pulmonary catheter data, hemoglobin/hematocrit, platelets, sedimentation rate, and urine analysis. Moreover, I would consider obtaining an echocardiogram and perform a funduscopic examination, to look for the presence of retinal fat emboli.

*Gurd AR, Wilson RI: The fat embolism syndrome, J Bone Joint Surg Br 56:408-416, 1974.

8) Assuming this is fat emboli syndrome (FES), what would you do?

UBP Answer: I would administer 100% oxygen, treat his hypotension, correct any hypovolemia, replace blood and platelets as required, continue mechanical ventilation, monitor the patient carefully for further deterioration, and inform the surgeon of his condition (i.e. the surgeon may choose to switch from intramedullary nailing to external fixation of the femur).



Post-operative Management


1) The following day the PaO2 is 68 mmHg with a FiO2 of 50% and the CXR shows bilateral diffuse infiltrates. What do you think might be going on?

UBP Answer: These results are consistent with Acute Respiratory Distress Syndrome (ARDS), which is most likely a consequence of his fat embolism syndrome, (although head trauma can also lead to ARDS). Moreover, if blood were transfused, I would also consider the possibility of TRALI.

ARDS represents the pulmonary manifestation of the systemic inflammatory response syndrome (SIRS). There is injury to the capillary alveolar membrane resulting in bilateral diffuse infiltrates, severe dyspnea, and hypoxemia secondary to intrapulmonary shunting. The syndrome may lead to fibrosing alveolitis and permanent scarring of the lungs.


2) What is required for the diagnosis of ARDS?

UBP Answer: The diagnosis requires an identifiable cause, acute onset, diffuse bilateral infiltrates on CXR, a PaO2 to FiO2 ratio of less than 200, and a PAOP below 18 mmHg or no clinical evidence of left atrial hypertension.

3) What is the recommended treatment?

UBP Answer: Treatment includes aggressively treating causative events and reversible pathology such as DIC, sepsis, or hypotension; avoiding complications; and supportive mechanical ventilation. Mechanical ventilation should provide sufficient PEEP to recruit collapsed alveoli and improve gas exchange while avoiding high airway pressures and large tidal volumes (tidal volumes 6 ml/kg or less & and static airway pressures < 30 cm H2O). Permissive hypercapnia may be necessary to avoid higher tidal volumes and airway pressures. The FiO2 should be less than 50% if possible to prevent iatrogenic lung injury. While inhaled nitric oxide, inhaled prostacyclin, high-frequency ventilation, inverse ratio ventilation, and ventilation in the prone position have all been shown to temporarily improve oxygenation, none have provided significant long term outcome differences when compared with standard ventilation strategies.

4) The surgery resident recommends steroids, PEEP, and 10 ml/kg tidal volume. What do you think of this recommendation?

UBP Answer: Giving steroids early in ARDS has been associated with an increase in mortality, although some small trials have shown reduced mortality when they are administered during the fibroproliferative phase of ARDS occurring around days 4-10. PEEP may be helpful in recruiting healthy alveoli, although the long term benefits are unproven. A tidal volume of 10 ml/kg is too high and may result in volutrauma or barotrauma to healthy lung. In fact, lower tidal volumes and airway pressures are the only intervention proven to reduce mortality in patients with ARDS.

5) On post-op day 5 the patient’s serum sodium is 129 mEq/L and the urinary sodium is 105 mEq/L. What do you think might be going on?

UBP Answer: A high urinary sodium and serum hyponatremia are consistent with both cerebral salt wasting syndrome (CSWS) and syndrome of inappropriate antidiuretic hormone (SIADH). Either of these two disorders may occur following TBI and may be best differentiated by the volume status of the patient. CSWS is usually associated with hypovolemia, while patients with SIADH are usually euvolemic.

6) How can you tell the difference between CSWS and SIADH?

UBP Answer: As I mentioned before, CSWS is usually associated with hypovolemia whereas patients with SIADH are euvolemic. In addition, patients with SIADH exhibit elevated ADH levels and rarely develop urine sodium levels > 100 mEq/L. Patients with CSWS usually have normal ADH levels and often develop urine sodium levels > 100 mEq/L.

7) Is it important to distinguish between the two?

UBP Answer: It is important because the treatment for SIADH includes water restriction along with diuresis, demeclocycline (which inhibits ADH effects on renal tubules), and sodium replacement. On the other hand, this treatment would be inappropriate for a patient with CSWS, as water restriction and diuresis could exacerbate the hypovolemia associated with this disorder.

Key Topics and Clinical Considerations


1. Acute Respiratory Distress Syndrome (ARDS)
a. A Practice of Anesthesia for Infants and Children (Cote): (pages 414-415)
b. Anesthesia and Co-Existing Disease – 5th Ed.: (pages 184-191)
c. Anesthesiology – 6th Ed. (Yao): (pages 55-71, 1174, 1198-1199)
d. Chestnut’s Obstetric Anesthesia – 4th Ed.: (pages 637-642)
e. Clinical Anesthesia – 6th Ed. (Barash): (pages 894-895, 1456-1459)
f. Clinical Anesthesiology – 4th Ed. (Morgan & Mikhail): (pages 868, 1040-1043)
g. Evidence-Based Practice of Anesth. – 2nd Ed. (Fleisher): (Chapter 31)
h. Miller’s Anesthesia – 7th Ed.: (pages 2667, 2854-2860, 2889-2894)
i. The ICU Book – 2nd Ed. (Marino): (pages 371-385, 445, 704)

2. Airway Management / Difficult Airway
a. Anesthesiology – 6th Edition (Yao): (pages 993-1006)
b. Clinical Anesthesia – 6th Edition (Barash): (pages 751-789)
c. Clinical Anesthesiology – 4th Edition (Morgan & Mikhail): (pages 91-116)
d. Evidence-Based Practice of Anesthes. – 2nd Edition (Fleisher): (Chapters 17 & 18)
e. Miller’s Anesthesia – 7th Edition: (pages 1573-1608)

3. Basilar Skull Fracture
a. A Practice of Anesthesia for Infants and Children (Cote): (pages 523)
b. Clinical Anesthesia – 6th Ed. (Barash): (pages 891)
c. Clinical Anesthesiology – 4th Ed. (Morgan & Mikhail): (pages 639, 867)
d. Miller’s Anesthesia – 7th Ed.: (pages 2068)

4. Cerebral Salt Wasting Syndrome (CSWS)
a. Anesthesiology – 6th Ed. (Yao): (pages 601-602)
b. Clinical Anesthesia – 6th Ed. (Barash): (pages 305)
c. Miller’s Anesthesia – 7th Ed.: (pages 1708)
d. Thoracic Anesthesia – 3rd Ed. (Kaplan): (pages 16)

5. Cervical Spine Management in the Trauma Patient
a. A Practice of Anesthesia for Infants and Children (Cote): (pages 819)
b. Anesthesia and Co-Existing Disease – 5th Edition: (pages 239-241)
c. Chestnut’s Obstetric Anesthesia – 4th Edition: (pages 1154)
d. Clinical Anesthesia – 6th Edition (Barash): (pages 892-893)
e. Clinical Anesthesiology – 4th Edition (Morgan & Mikhail): (pages 862)
f. Miller’s Anesthesia – 7th Edition: (pages 2284)

6. Fat Embolism Syndrome
a. A Practice of Anesthesia for Infants and Children (Cote): (pages 634)
b. Anesthesia and Co-Existing Disease – 5th Ed.: (pages 193)
c. Clinical Anesthesia – 6th Ed. (Barash): (pages 1388-1389)
d. Clinical Anesthesiology – 4th Ed. (Morgan & Mikhail): (pages 850, 869)
e. Miller’s Anesthesia – 7th Ed.: (pages 2243-2244, 2301-2302)

7. Fluid Management
a. A Practice of Anesthesia for Infants and Children (Cote): (pages 159-174, 722-723, 823-824)
b. Clinical Anesthesia – 6th Edition (Barash): (pages 284-287, 296-304, 910-911, 1018, 1214-1215, )
c. Clinical Anesthesiology – 4th Edition (Morgan & Mikhail): (pages 690-697, 864-865, 936-937)
d. Evidence-Based Practice of Anesth. – 2nd Edition (Fleisher): (Chapter 30)
e. Miller’s Anesthesia – 7th Edition: (pages 1723-1735)
f. The ICU Book – 2nd Edition (Marino): (pages 207-240)

8. GERD / Full Stomach / Aspiration
a. A Practice of Anesthesia for Infants and Children (Cote): (pages 37-38, 583-584)
b. Anesthesia and Co-Existing Disease – 5th Edition: (pages 280-284)
c. Anesthesiology – 6th Edition (Yao): (pages 50-55, 1207)
d. Chestnut’s Obstetric Anesthesia – 4th Edition: (pages 633-650)
e. Clinical Anesthesia – 6th Edition (Barash): (pages 589-591, 1223-1224)
f. Clinical Anesthesiology – 4th Edition (Morgan & Mikhail): (pages 286-288, 833-835)
g. Evidence-Based Practice of Anesthes. – 2nd Edition (Fleisher): (Chapter 49)
h. Miller’s Anesthesia – 7th Edition: (pages 1062, 1583, 1605-1606, 2283-2284, 2574-2575)
i. Practice Guidelines for Preoperative Fasting and the Use of Pharmacologic Agents to Reduce the Risk of Pulmonary Aspiration: Application to Healthy Patients Undergoing Elective Procedures

9. Glasgow Coma Scale
a. A Practice of Anesthesia for Infants and Children (Cote): (pages 781, 824-825)
b. Anesthesia and Co-Existing Disease – 5th Ed.: (pages 223-224)
c. Anesthesiology – 6th Ed. (Yao): (pages 603-607, 996)
d. Chestnut’s Obstetric Anesthesia – 4th Ed.: (pages 1151)
e. Clinical Anesthesia – 6th Ed. (Barash): (pages 899-900, 1023)
f. Clinical Anesthesiology – 4th Ed. (Morgan & Mikhail): (pages 639-640)
g. Miller’s Anesthesia – 7th Ed.: (pages 2279-2280)
h. The ICU Book – 2nd Ed. (Marino): (pages 784-785)

10. Head Injury / Traumatic Brain Injury
a. A Practice of Anesthesia for Infants and Children (Cote): (pages 522-523)
b. Anesthesia and Co-Existing Disease – 5th Edition: (pages 223-225)
c. Anesthesiology – 6th Ed. (Yao): (pages 597-616)
d. Chestnut’s Obstetric Anesthesia – 4th Edition: (pages 1155-1156)
e. Clinical Anesthesia – 6th Edition (Barash): (pages 898-901, 1008, 1022-1025, 1447-1449)
f. Clinical Anesthesiology – 4th Edition (Morgan & Mikhail): (pages 639-641)
g. Miller’s Anesthesia – 7th Edition: (pages 2068-2072)

11. Intracranial Hypertension / Brain Protection
a. A Practice of Anesthesia for Infants and Children (Cote): (pages 509-522)
b. Anesthesia and Co-Existing Disease – 5th Edition: (pages 202-205)
c. Clinical Anesthesia – 6th Edition (Barash): (pages 229, 302, 1008, 1014-1019)
d. Clinical Anesthesiology – 4th Edition (Morgan & Mikhail): (pages 623-624, 632)
e. Evidence-Based Practice of Anesth. – 2nd Edition (Fleisher): (Chapters 64 & 65)
f. Miller’s Anesthesia – 7th Edition: (pages 2045-2062)

12. Obesity
a. Anesthesia and Co-Existing Disease – 5th Edition: (pages 297-310)
b. Anesthesiology – 6th Edition (Yao): (pages 1249-1282)
c. Chestnut’s Obstetric Anesthesia – 4th Edition: (pages 1079-1090)
d. Clinical Anesthesia – 6th Edition (Barash): (pages 1230-1245)
e. Clinical Anesthesiology – 4th Edition (Morgan & Mikhail): (pages 813-815)
f. Evidence-Based Practice of Anesth. – 2nd Edition (Fleisher): (Chapter 38)
g. Miller’s Anesthesia – 7th Edition: (pages 2089-2104)

13. Syndrome of Inappropriate Antidiuretic Hormone (SIADH)
a. A Practice of Anesthesia for Infants and Children (Cote): (pages 174, 522, 548-549)
b. Anesthesiology – 6th Ed. (Yao): (pages 601-602)
c. Clinical Anesthesia – 6th Ed. (Barash): (pages 304-309, 1302)
d. Clinical Anesthesiology – 4th Ed. (Morgan & Mikhail): (pages 672)
e. Miller’s Anesthesia – 7th Ed.: (pages 1093-1094, 1707-1708, 2063, 2677-2678, 2912)
f. The ICU Book – 2nd Ed. (Marino): (pages 643)

14. Temperature: Hypothermia
a. A Practice of Anesthesia for Infants and Children (Cote): (pages 210, 406, 461, 519, 557-567, 644, 649, 738. 751, 1019)
b. Anesthesia and Co-Existing Disease – 5th Ed.: (pages 474, 584)
c. Anesthesiology – 6th Ed. (Yao): (pages 173-175, 264, 398-399, 612, 821, 842, 1129, 1149)
d. Chestnut’s Obstetric Anesthesia – 4th Ed.: (pages 768, 158, 164, 201, 616, 832)
e. Clinical Anesthesia – 6th Ed. (Barash): (pages282-283, 711-712, 827-828, 1190-1191)
f. Clinical Anesthesiology – 4th Ed. (Morgan & Mikhail): (pages 148-150)
g. Evidence-Based Practice of Anesth. – 2nd Ed. (Fleisher): (Chapter 33)
h. Miller’s Anesthesia – 7th Ed.: (pages 1533-1550, 2564, 2941-2942)
i. The ICU Book – 2nd Ed. (Marino): (pages 649)
j. Thoracic Anesthesia – 3rd Ed. (Kaplan): (pages 323, 330)

15. Trauma Patient
a. A Practice of Anesthesia for Infants and Children (Cote): (pages 781-783, 815-832)
b. Anesthesia and Co-Existing Disease – 5th Edition: (pages 131-133)
c. Anesthesiology – 6th Edition (Yao): (pages 1134-1154)
d. Chestnut’s Obstetric Anesthesia – 4th Edition: (pages 1149-1161)
e. Clinical Anesthesia – 6th Edition (Barash): (pages 889-923)
f. Clinical Anesthesiology – 4th Edition (Morgan & Mikhail): (pages 861-870)
g. Miller’s Anesthesia – 7th Edition: (pages 2277-2307)


To purchase more detailed questions and answers for the oral boards from The Ultimate Board Prep click here
  Posting rules

     To view or add comments you must be a registered user and login



 
All rights reserved © 2018. Designed by AnaesthesiaUK.

{Site map} {Site disclaimer} {Privacy Policy} {Terms and conditions}

 Like us on Facebook 

vp