Trauma in the pediatric patient Flashcards

1
Q

What is pseudotumor cerebri?

A

idiopathic intracranial hypertension (IIH), is defined as intracranial hypertension (usually >
20 mmHg) that is associated with normal CSF composition, normal sensorium, and the
absence of a mass lesion.
Normally in obese women, but can happen in children. Can cause headache, visual disturbances and even blindness

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2
Q

Treatment for pseudotumor cerebri:

A

includes: (1) carbonic anhydrase inhibitors (i.e. acetazolamide) to
decrease CSF production; (2) furosemide (used when carbonic anhydrase inhibitors or not
tolerated or are ineffective); (3) corticosteroids to reduce ICP when symptoms are severe
(mechanism unknown); (4) serial lumbar punctures to remove CSF; (5) insertion ofa
ventriculoperitoneal shunt,

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3
Q

You can’t get access in pedi pt: wyd?

A

If I were unable to obtain access through the anticubital fossa or by direct
percutaneous cannulation of the femoral veins, I would consider placing an intraosseous
infusion device in the tibial plateau. You could also have surgeon cut down to femoral or saphenous vein .
remember-if pt has c collar you clearly can’t place IV in neck

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4
Q

Pedi pt GCS is 8 (head trauma). How are you handling the airway?

A

ensure the presence of the appropriate airway equipment (the presence of a C-
collar and the need for cricoid pressure and inline stabilization may make intubation more difficult-this is how you’re saying you want a glide or FOB)(2) position the patient in 30° reverse-trendelenburg, if hemodynamically toleratedpre-oxygenate the patient with
100% oxygen; ( 4) apply manual in-line stabilization of the cervical spine (traumatic brain
injury with C-collar in place); (5) administer fentanyl and/or lidocaine to reduce the effects of
laryngoscopy on ICP; (6) provide atropine to avoid reflex-induced bradycardia during
laryngoscopy (should also be considered when utilizing succinylcholine); (7) and perform a
rapid sequence induction utilizing etomidate (improved hemodynamic stability; decreased
CMR02 and CBF) and high dose rocuronium (succinylcholine would be less desirable due to
risk of hyperkalemia in male children< 8 years of age).

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5
Q

What bothers you about somnolence in neuro pts?

DDX:

A

altered mental state places him at increased risk for aspiration and inadequate ventilation,
with the latter potentially resulting in further increases in ICP (secondary to hypercarbia
and/or hypoxia).
DDX:(1) trauma-induced cerebral hemorrhage and/or edema (significant enough to overwhelm the
ability of the shunt to compensate); (2) ventriculoperitoneal shunt malfunction (i.e. partial or
complete obstruction); (3) seizure (postictal state); (4) significant anemia secondary to occult
bleeding that has not yet been identified (i.e. thoracic, abdominal, or long bone fracture); (5)
hyponatremia; and ( 6) hypoglycemia.

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6
Q

Let’s do this again: with elevated ICP, what are you going to do to reduce ICP?

A

Secure airway and ensure adequate oxygenation and ventilation ensuring that there is no venous obstruction (especially with a C-
collar in place);elevating his head 15-30 degrees to facilitate venous drainage (if

hemodynamically tolerated); (4) verifying that his ventriculoperitoneal shunt is functioning
properly (function can sometimes be assessed when the device includes an extracranial
subcutaneous compressible bulb); (5) administering analgesics (i.e. opioids) and sedatives
(i.e. benzodiazepines) to reduce the elaboration of excitory neurotransmitters; (6) giving
mannitol and a diuretic (i.e. furosemide) to reduce the fluid in the brain also emergent crani

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7
Q

Why is hyperventilation not a first line thing in TBI?

A

While hyperventilation would reduce his ICP by inducing cerebral vasoconstriction, this
is no longer recommended in the setting of traumatic brain injury 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).

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8
Q

Since he has pseudotumor cerebri, would you just perform a lumbar puncture to
remove some CSF?

A

While the drainage of CSF via lumbar puncture is often utilized to treat
symptomatic pseudotumor cerebri, it would be inappropriate in a patient with recent head
trauma and an altered level of consciousness without first obtaining a CT of the head to
identify the presence of unequal pressures between the supratentorial and infratentorial
compartments. My concern is that, in the presence of a space-occupying lesion (i.e.
expanding hematoma), the creation of a low resistance outlet for CSF in the lumbar spine
may lead to a dangerous pressure gradient between the cerebral and spinal compartments,
placing the patient at risk for trans-tentorial or uncal herniation. Moreover, ifl believed that
the patient was at increased risk for coagulopathy, I would want to order additional lab work
and perform a careful physical exam to rule out this condition.

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9
Q

Trauma (head) pt bp drops from 107/76 to 68/42

A

(1) hemorrhagic shock, secondary to unrecognized occult
bleeding (i.e. thoracic, abdominal, or extremity injury); (2) neurogenic shock, secondary to
cervical spinal cord injury; (3) tension pneumothorax, secondary to trauma or central line
placement (potentially worsened with mechanical ventilation); (4) cardiac tamponade,
secondary to his traumatic fall; (5) fat embolism, secondary to an unrecognized long bone
fracture; and (6) anaphylaxis.

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10
Q

What is the FAST exam?

A

Focused Assessment with Sonography for Trauma (FAST)ultrasound examination utilized primarily in hemodynamically unstable blunt trauma patients
to quickly determine whether there is blood present within the peritoneum, pericardium, and
thorax. While the exam provides a safe, rapid, inexpensive, noninvasive, and radiation-free
method for evaluation of the abdomen, it is more user-dependent than CT fails to identify retroperitoneal and diaphragmatic injuries, CT preferred in hemodynamically stable patient

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11
Q

abdominal compartment syndrome and what it does to the liver? What can it lead to as far as ventilation, cardiovascular, and ICP?

A

Reduced perfusion of the liver can lead to an inability to metabolize
lactate, altered drug metabolism (delayed), and impaired synthesis of coagulation factors.Furthermore, increased abdominal pressures can lead to: (1) impaired ventilation, secondary
to cephalad displacement of the diaphragm and decreased functional residual capacity; (2)
cardiovascular depression, secondary to decreased venous returnincreased ICP in association with
decreased cerebral perfusion (the increase in ICP is possibly secondary to decreased cerebral
venous outflow

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12
Q

Diagnosis of abdominal compartment syndrome:

A

abdominal pain and distention are commonly present (not always),
dyspnea and reduced urine output are often the earliest signs of developing intra-abdominal
hypertension.intra-abdominal pressure, which can be
indirectly measured via a nasogastric tube in the stomach or a Foley catheter in the bladder
(intravesicular pressure). Intra-abdominal pressures exceeding 20-25 mm Hg are considered
to be critical, but abdominal compartment syndrome may occur at pressures above 10 mm

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13
Q

So, surgeon wants to go back for ab compartment syndrome-what workup do you want? (trauma pt)

A

KIM that occult bleeding may be the cause of his condition. and can cause electrolyte imbalances and fluid losses as well as end organ damage. complete blood count, blood

type and cross match, basic metabolic profile, liver and renal function tests, and a
coagulation profile. Given the significant risk of cardiopulmonary compromise and
worsening hemodynamic instability during surgery, I would take the following steps as time
allowed: (1) administer blood and fluids to replace losses and correct any electrolyte
imbalances, keeping in mind that overaggressive fluid administration could potentially
exacerbate the abdominal compartment syndrome (consider using colloids, rather than
crystalloids to reduce the risk of exacerbating abdominal compartment syndrome); (2) ensure
adequate muscle relaxation (abdominal muscle tone may contribute to increased abdominal
compartment pressures); (3) order a chest radiograph, to better evaluate the severity of any
pulmonary compromise; (4) order an echocardiogram to assess his cardiac contractility and
volume status; and (5) ensure that additional blood products, vasopressors, and inotropes
were available in the operating room prior to induction.

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14
Q

What measurement is falsely elevated in abdominal compartment syndrome?

A

CVP-so, KIM when evaluating this value in the presence of abdominal compartment syndrome

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15
Q

Can you use TEE in children?

A

Yes-to monitor cardiac function, and aid in fluid mgmt

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16
Q

So, you think you should place an NG tube prior to induction in this full stomach pt wiht facial fractures and facial trauma?

A

no. could have basilar skull fracture, and also be careful-placing that tube can cause distress and increase ICP. Just think about what you’re saying and be careful

17
Q

Ab compartment syndrome surgery: once surgeon makes incison, pts BP drops to 63/38-what do you think is going on?

A

Given the timing of this event, his hypotension is most likely secondary to the
release of cardiodepressant factors with the reperfusion of ischemic tissue. Other potential
causes or contributing factors would include the loss of intravascular volume with the release
of abdominal tamponade (i.e. blood and/or fluid), inadequate preoperative fluid replacement,
and excessive anesthetic (induction and/or maintenance). I would also consider other
possible causes such as tension pneumothorax (central line placement, trauma), critically
increased ICP with subsequent autonomic instability, cardiac tamponade (trauma),
anaphylaxis, and arrhythmia.

18
Q
Young kid (7 yo) trauma pt:For the sake of discussion, assume that the
patient's blood type is not yet known. The blood bank wishes to switch to Rh(D)
positive PRBCs to preserve inventory of Rh(D) negative PRBCs. Are you ok with this?
A

Recognizing that this is a male patient and that it is sometimes necessary to
preserve a limited supply ofRh(D) negative PRBCs (for Rh(D)-negative female patients and
females whose blood type is unknown), I would probably agree to the switch. However, Iwould first want to ask about any history of previous exposure to Rh(D) positive PRBCs,
recognizing that a previous exposure could lead to a hemolytic reaction (delayed transfusion
reaction). If it was later determined that the patient was Rh(D) negative, I would also
consider providing him with Rhogam within 72 hours, and let the mother know that, if possible, he should be checked for anti-D antibodies prior to allowing a subsequent Rh-
positive transfusion.

19
Q

Do platelets have to be ABO compatible?

A

The platelets in apheresis packs should be ABO compatible since they are
suspended in plasma containing anti-A and anti-B isoagglutinins, placing any recipient of a
non-ABO compatible transfusion at risk for hemolysis (especially in the case of a donor with
high titer isoagglutinins). The administration of non-ABO compatible whole blood-derived
platelets, on the other hand, does not result in clinically significant hemolysis in adults, due
to the limited amount of plasma involved (small children should receive ABO compatible
platelets regardless of whether they are whole blood-derived or collected via apheresis).
Rh(D) antigen matching is desirable when red blood cells are present (red blood cells may
express Rh antigens), placing the patient at risk for Rh(D) alloimmunization (mostly a
problem for Rh(D) negative females with child-bearing potential). Therefore, matching for
Rh(D) antigen is unnecessary for apheresis platelets, which contain almost no red blood cells.
However, Rh(D) matching is preferable when utilizing whole blood-derived platelets, which
may contain enough red blood cells to provoke Rh alloimmunization. Rh immune globulin
(Rhogam) may be administered within 72 hours when unmatched, whole blood-derived,
platelets are administered to a female patient with child-bearing potential.

20
Q

If you were to administer fresh frozen plasma, what should be the donor typing?

A

Since fresh frozen plasma (FFP) may contain anti-A and anti-B
isoagglutinins, it should be ABO compatible with the recipient’s red blood cells to prevent
hemolysis. If the recipient’s blood type is unknown, it is safe to transfuse with FFP from a
donor with AB blood type, since the plasma of this donor would not contain anti-A or anti-B
isoagglutinins. Furthermore, since FFP does not contain any red blood cells, Rh(D) matching
is not necessary to prevent Rh alloimmunization.

21
Q

If you were to administer fresh frozen plasma, what should be the donor typing? Is RhD matching necessary?

A

Since fresh frozen plasma (FFP) may contain anti-A and anti-B
isoagglutinins, it should be ABO compatible with the recipient’s red blood cells to prevent
hemolysis. If the recipient’s blood type is unknown, it is safe to transfuse with FFP from a
donor with AB blood type, since the plasma of this donor would not contain anti-A or anti-B
isoagglutinins. Furthermore, since FFP does not contain any red blood cells, Rh(D) matching
is not necessary to prevent Rh alloimmunization.

22
Q

You are transfusing PRBCs and FFP when you notice a prolonged QT interval. Why does this happen? What
would you do?

A

Assuming this prolonged QT interval was not present prior to the transfusion
of citrate-containing blood products (especially FFP, which contains significantly more
plasma), the most likely cause is citrate-induced hypocalcemia. Therefore, I would look
for other signs ofhypocalcemia, such as hypotension and myocardial depressionThe rapid transfusion of FFP can overwhelm the liver’s capacity to metabolize citrate,
especially when administered through a central line (reduced time for dilution of the FFP
prior to entering the heart and coronary vessels - may be better to administer FFP through a
peripheral line) in the setting ofhypotension.
I would d/c admin of FFP
Monitor EKG

correct any hypomagnesemia (rapid blood
transfusion may cause hypomagnesemia, and the treatment of hypocalcemia is ineffective in
the setting ofhypomagnesemia) or hyperkalemia (potentiates hypocalcemia-induced cardiac
and neuromuscular irritability), and/or metabolic or respiratory alkalosis; (4) administer 10-
20 mg/kg of calcium chloride (1 mL of 10% solution= 100 mg calcium chloride= 27 mg
elemental calcium) or calcium gluconate (1 mL of 10% solution = 100 mg calcium gluconate
= 9 mg elemental calcium) through a large peripheral or central vein (both drugs can cause
significant local vasoconstriction with subsequent tissue necrosis); and (5) correct any
hypokalemia and/or acidosis after normalizing his calcium levels.

23
Q

Should you fix hypokalemia before normalization of calcium levels? SHOULD you correct metabolic/and or resp acidosis before fixing calcium?

A

The correction of hypokalemia prior to the normalization of calcium levels should be
avoided, since hypokalemia has a protective affect against hypocalcemic tetany.Correcting metabolic and/or respiratory acidosis should be delayed until calcium
replacement has been initiated, since hyperventilation and/or bicarbonate administration
can exacerbate the symptoms ofhypocalcemia

24
Q

Would you give a propofol infusion to a child?

A

I would not use an intravenous infusion of propofol to maintain continuous
sedation for this pediatric patient. My concern is that there is increasing evidence that the
continuous infusion of high dose propofol ( 4-5 mg/kg/hr) for long periods ohime (usually
cited as 24-48 hours; some case reports suggest developing propofol infusion syndrome after
only 5-6 hours) may lead to a syndrome associated with lethal metabolic acidosis, called
propofol infusion syndrome (PRIS).

25
Q

What is propofol infusion syndrome?

A

Propofol infusion syndrome primarily occurs in children and critically ill
adult patients following the continuous infusion of high dose propofol over a prolonged
period of time. PRIS often presents with the acute onset of refractory bradycardia in
association with metabolic acidosis, rhabdomyolysis, lipemia, hyperkalemia, hepatomegaly,
fatty liver, renal failure, and cardiomyopathy. The end result is cardiovascular collapse that
is refractory to resuscitative efforts.

26
Q

Risk factors for PRIS?

A

In addition to the prolonged infusion of high-dose
propofol, the risk factors for developing this syndrome include: ( 1) a defect in lipid
metabolism (including some forms of mitochondrial disease); (2) serious neurologic injury;
(3) sepsis; (4) concomitant infusion of catecholamines and/or inotropes; and (5) the
administration of high-dose corticosterioids. Treatment is primarily supportive, following
the discontinuation of propofol infusion; the mortality rate is around 80%

27
Q

Wyd if you think there may be child abuse?

A

If I suspected that his scars were the result of child abuse, I would look for
other findings consistent with child abuse, such as: (1) bruises or bums in the shape of
objects; (2) soft tissue or genital bruises; (3) unexplained mouth and/or dental injuries; (4)
signs of neglect (e.g. poor hygiene or height and weight less than the 5th percentile); (5)
multiple fractures of various ages (order a skeletal survey of the skull, ribs, and all long
bones); ( 6) retinal hemorrhages on funduscopic exam; (7) the character and extent of injury
not well explained by the offered history; and (8) a delay in seeking medical care. Moreover,I would keep in mind that physically and mentally handicapped children are more likely to be
abused, and consider the possibility that this child’s injuries may have occurred secondary to
abuse rather than the reported fall (abdominal and head injuries are common findings).
Finally, I would write a detailed note in the chart reflective of my findings and report my
concerns to the appropriate authorities.

28
Q

Mom asks you not to tell about signs of child abuse

A

I would explain to her that I understand her concerns and that I am not
questioning her love for her child, but that I am ethically and legally obligated to report
suspected or known child abuse.

29
Q

Extrernal ventricular drain shunt falls from bed to floor-does this concern you?

A

I would be very concerned, because significantly changing the height of an
open drainage bag in relation to the child’s head places him at risk for sudden and dangerous
changes in intracranial pressure. In this case, the rapid loss of intracranial CSF as it drains
into the suddenly lowered drainage bag places the child at risk for ventricular collapse and
ruptured cortical veins. For this reason, the anesthesiologist should consider clamping the
ventriculostomy tubing during the transport of patients with external ventricular drains.

30
Q

What is slit ventricle syndrome?

A

This is a condition that may develop when excessive CSF shunting occurs
concomitantly with brain growth, leading to irreversibly collapsed ventricles (brain grows to
fill the relatively empty ventricles) and decreased intracranial compliance. These stiff and
noncompliant ventricles place the patient at risk for cerebral herniation due to an inability to
adequately compensate for changes in intracranial volume (i.e. blood, CSF, and/or edema).
Therefore, it is important to identify this subset of patients (i.e. CT scan) and avoid factors
that could contribute to significant changes in intracranial volume (i.e. excessive
administration ofhypotonic fluids).