UBP 6.2 (Short Form): Trauma – Pediatric Patient Flashcards
Secondary Subject -- Pseudotumor Cerebri / Ventriculoperitoneal Shunt / Head Injury / Intracranial Hypertension / FAST exam (Focused Assessment with Sonography for Trauma) / Abdominal Compartment Syndrome / Transfusion Medicine – ABO compatibility and Rh(D) status / Hypocalcemia - Citrate Toxicity / Propofol Infusion Syndrome (PRIS) / Child Abuse / Slit Ventricle Syndrome
What is Pseudotumor Cerebri?
(A 7-year-old male presents to the trauma suite after falling from a height of eight feet when playing on a jungle gym. The child appears to have suffered some facial trauma, has a cervical collar in place, and is somnolent. His mother reports that he has a ventriculoperitoneal shunt to treat pseudotumor cerebri. There is no vascular access. Vital Signs: P = 139, R = 26, BP = 138/76 mmHg, O2 sat = 98% on non-rebreathing mask, T = 35.4 °C)
- (UBP Live Course Notes –*
- What is it? How does it present? How do you treat?)*
Pseudotumor cerebri, also known as benign intracranial hypertension or 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.
The condition typically occurs in obese women of child-bearing age, but can occur in young children such as this patient.
The syndrome may result in – headaches, visual disturbances, papilledema, and even blindness (the latter is due to optic atrophy).
Treatment includes:
- carbonic anhydrase inhibitors
- (i.e. acetazolamide) to decrease CSF production;
- furosemide
- (used when carbonic anhydrase inhibitors are not tolerated or are ineffective);
- corticosteroids to reduce ICP when symptoms are severe (mechanism unknown);
- serial lumbar punctures to remove CSF;
- insertion of a lumboperitoneal shunt (high rate of failure), ventriculoperitoneal shunt, or ventriculoatrial shunt (it is easier to monitor the shunt function of the latter two, due to the presence of an extracranial subcutaneous compressible bulb); and
- optic nerve sheath fenestration, to relieve pressure around the optic nerve.
Two attempts have been made at obtaining intravascular access without success.
What will you do?
(A 7-year-old male presents to the trauma suite after falling from a height of eight feet when playing on a jungle gym. The child appears to have suffered some facial trauma, has a cervical collar in place, and is somnolent. His mother reports that he has a ventriculoperitoneal shunt to treat pseudotumor cerebri. There is no vascular access. Vital Signs: P = 139, R = 26, BP = 138/76 mmHg, O2 sat = 98% on non-rebreathing mask, T = 35.4 °C)
If I were unable to obtain access through the antecubital fossa or by direct percutaneous cannulation of the femoral veins, I would –
consider placing an intraosseous infusion device in the tibial plateau (slightly medial to a spot 2 cm below the tibial tuberosity) to provide a route for resuscitative fluids and medications while obtaining more definitive access via surgical cut-down to the femoral or saphenous vein (femoral vein is located just below the inguinal ligament; saphenous vein located just below the inguinal ligament or at the ankle).
Given the presence of a C-collar and my reluctance to obstruct personnel managing the airway, I would avoid attempting to obtain access via the subclavian or internal jugular veins, if possible.
His Glasgow Coma Scale score is 8.
How will you manage this patient’s airway?
(A 7-year-old male presents to the trauma suite after falling from a height of eight feet when playing on a jungle gym. The child appears to have suffered some facial trauma, has a cervical collar in place, and is somnolent. His mother reports that he has a ventriculoperitoneal shunt to treat pseudotumor cerebri. There is no vascular access. Vital Signs: P = 139, R = 26, BP = 138/76 mmHg, O2 sat = 98% on non-rebreathing mask, T = 35.4 °C)
Given his recent head trauma, decreased level of consciousness (low Glasgow Coma Scale score), and full stomach (trauma patient),
I would want to secure his airway with an endotracheal tube in order to avoid aspiration and/or inadequate ventilation, with the latter potentially leading to increased ICP and worsening mental status (secondary to hypercapnia and hypoxemia).
Therefore, I would quickly evaluate the airway and, assuming the exam was reassuring (i.e. the facial trauma did not appear to involve or affect the airway), I would:
- 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);
- position the patient in 30° reverse-trendelenburg, if hemodynamically tolerated (facilitate venous drainage from the head, facilitate rapid intubation, improve respiratory mechanics, and reduce the risk of passive regurgitation);
- pre-oxygenate the patient with 100% oxygen;
- apply manual in-line stabilization of the cervical spine (traumatic brain injury with C-collar in place);
- administer fentanyl and/or lidocaine to reduce the effects of laryngoscopy on ICP;
- provide atropine to avoid reflex-induced bradycardia during laryngoscopy
- (should also be considered when utilizing succinylcholine); and
- perform a rapid sequence induction utilizing –
- etomidate
- (improved hemodynamic stability; decreased CMRO2 and CBF) and
- high dose rocuronium
- (succinylcholine would be less desirable due to risk of hyperkalemia in male children < 8 years of age).
- etomidate
My primary goals during this process are –
- to maintain adequate cerebral perfusion and
- avoid aspiration, cervical spine injury, and those factors that could lead to increased ICP, such as – hypoxia, hypercarbia, and sympathetic stimulation.
What do you think about this patient’s somnolence?
(A 7-year-old male presents to the trauma suite after falling from a height of eight feet when playing on a jungle gym. The child appears to have suffered some facial trauma, has a cervical collar in place, and is somnolent. His mother reports that he has a ventriculoperitoneal shunt to treat pseudotumor cerebri. There is no vascular access. Vital Signs: P = 139, R = 26, BP = 138/76 mmHg, O2 sat = 98% on non-rebreathing mask, T = 35.4 °C)
His somnolence is very concerning because – it may be the result of an underlying process that leads to significant neurologic injury or even death.
Moreover, his 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).
Therefore, I would – secure the airway and stabilize the patient, while at the same time attempting to identify the cause of his mental state, so that the appropriate treatment could be initiated.
Some of the potential causes of his somnolence would include:
- trauma-induced cerebral hemorrhage and/or edema
- (significant enough to overwhelm the ability of the shunt to compensate);
- ventriculoperitoneal shunt malfunction
- (i.e. partial or complete obstruction);
- seizure (postictal state);
- significant anemia secondary to occult bleeding that has not yet been identified (i.e. thoracic, abdominal, or long bone fracture);
- hyponatremia; and
- hypoglycemia.
If you believed his somnolence was due to elevated intracranial pressures, what would you do?
(A 7-year-old male presents to the trauma suite after falling from a height of eight feet when playing on a jungle gym. The child appears to have suffered some facial trauma, has a cervical collar in place, and is somnolent. His mother reports that he has a ventriculoperitoneal shunt to treat pseudotumor cerebri. There is no vascular access. Vital Signs: P = 139, R = 26, BP = 138/76 mmHg, O2 sat = 98% on non-rebreathing mask, T = 35.4 °C)
There are several actions I would take to reduce his ICP including:
- securing the airway to ensure adequate ventilation and oxygenation (maintaining his PaCO2 around 35-40 mmHg;
- 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);
- verifying that his ventriculoperitoneal shunt is functioning properly (function can sometimes be assessed when the device includes an extracranial subcutaneous compressible bulb);
- administering analgesics (i.e. opioids) and sedatives (i.e. benzodiazepines) to reduce the elaboration of excitatory neurotransmitters;
- giving mannitol and a diuretic (i.e. furosemide) to reduce the fluid in the brain; and
- administering a barbiturate (i.e. pentobarbital) to reduce ICP and CMRO2 (assuming this would be hemodynamically tolerated).
If these measures were unsuccessful, I would –
- consider administering a bolus of hypertonic saline (assuming his sodium level was < 150 mEq/L and his serum osmolality was < 300 mOsm/L).
As a last resort, a rescue craniotomy may be considered.
- Clinical Note:*
- 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).
Since he has pseudotumor cerebri, would you just perform a lumbar puncture to remove some CSF?
(A 7-year-old male presents to the trauma suite after falling from a height of eight feet when playing on a jungle gym. The child appears to have suffered some facial trauma, has a cervical collar in place, and is somnolent. His mother reports that he has a ventriculoperitoneal shunt to treat pseudotumor cerebri. There is no vascular access. Vital Signs: P = 139, R = 26, BP = 138/76 mmHg, O2 sat = 98% on non-rebreathing mask, T = 35.4 °C)
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, if I 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.
His blood pressure drops from 107/76 mmHg to 68/42 mmHg.
What do you think may be going on?
(A 7-year-old male presents to the trauma suite after falling from a height of eight feet when playing on a jungle gym. The child appears to have suffered some facial trauma, has a cervical collar in place, and is somnolent. His mother reports that he has a ventriculoperitoneal shunt to treat pseudotumor cerebri. There is no vascular access. Vital Signs: P = 139, R = 26, BP = 138/76 mmHg, O2 sat = 98% on non-rebreathing mask, T = 35.4 °C)
There are number of things that I would be considering as potential causes of his hypotension, including:
- hemorrhagic shock, secondary to unrecognized occult bleeding (i.e. thoracic, abdominal, or extremity injury);
- neurogenic shock, secondary to cervical spinal cord injury;
- tension pneumothorax, secondary to trauma (rib fracture) or central line placement (potentially worsened with mechanical ventilation);
- cardiac tamponade, secondary to his traumatic fall;
- fat embolism, secondary to an unrecognized long bone fracture; and
- anaphylaxis.
Furthermore, recognizing that the treatment of pseudotumor cerebri often includes steroid administration (a short course of high-dose corticosteroids is often utilized for patients with severe symptoms and/or a poor response to standard therapy), I would consider the possibility that –
- adrenal insufficiency is the cause of his hypotension.
- *Note: Pseudotumor cerebri patients may be on steroids.
What is the FAST exam?
(A 7-year-old male presents to the trauma suite after falling from a height of eight feet when playing on a jungle gym. The child appears to have suffered some facial trauma, has a cervical collar in place, and is somnolent. His mother reports that he has a ventriculoperitoneal shunt to treat pseudotumor cerebri. There is no vascular access. Vital Signs: P = 139, R = 26, BP = 138/76 mmHg, O2 sat = 98% on non-rebreathing mask, T = 35.4 °C)
The Focused Assessment with Sonography for Trauma (FAST) is – an 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 diagnostic peritoneal lavage (DPL) or CT,
- fails to identify retroperitoneal and diaphragmatic injuries,
- poorly identifies solid organ injury, and
- offers only moderate sensitivity (specificity is good).
Therefore, computed tomography (CT), which is capable of evaluating the retroperitoneum and identifying solid organ and diaphragmatic injury, is the preferred method of evaluation in the hemodynamically stable patient.
Clinical Notes:
- The FAST exam is utilized to evaluate four specific areas of the abdomen for free fluid, including the pericardium (subxiphoid), the hepatorenal recess (right upper quadrant), the perisplenic space (left upper quadrant), and the retrovesical pouch (superior to the pubic symphysis).
-
Diagnostic Peritoneal Lavage (DPL) is often used in the evaluation of hemodynamically unstable trauma patients following blunt or penetrating trauma.
- While it is the most sensitive test for hollow viscus and mesenteric injury, it fails to identify retroperitoneal and diaphragmatic injuries, and lacks organ specificity.
- This procedure has been largely replaced by the use of the FAST exam and computed tomography.
The FAST exam identifies free fluid in the abdomen, and you note increased abdominal girth and a tense abdomen.
What is the pathophysiology of abdominal compartment syndrome (ACS)?
(A 7-year-old male presents to the trauma suite after falling from a height of eight feet when playing on a jungle gym. The child appears to have suffered some facial trauma, has a cervical collar in place, and is somnolent. His mother reports that he has a ventriculoperitoneal shunt to treat pseudotumor cerebri. There is no vascular access. Vital Signs: P = 139, R = 26, BP = 138/76 mmHg, O2 sat = 98% on non-rebreathing mask, T = 35.4 °C)
When the accumulation of fluid, from edema (abdominal trauma, fluid overload, systemic inflammatory response syndrome) or blood (abdominal trauma), exceeds the abdominal wall compliance threshold,
intra-abdominal pressures increase rapidly.
When these pressure increase above the capillary perfusion pressure of intra-abdominal organs (around 20-25 mmHg), there are several detrimental effects, particularly involving the liver, kidneys, and bowel.
- Reduced perfusion of the liver can lead to an inability to metabolize lactate, altered drug metabolism (delayed), and impaired synthesis of coagulation factors.
- Decreased perfusion of the kidneys can result in oliguria or even anuria.
- Insufficient bowel perfusion can cause ileus, the translocation of bacterial products, lactate production, and the release of various mediators that can cause hemodynamic instability.
Furthermore, increased abdominal pressures can lead to:
- impaired ventilation, secondary to cephalad displacement of the diaphragm and decreased functional residual capacity;
- cardiovascular depression, secondary to –
- decreased venous return (cephalad movement of the diaphragm leads to increased thoracic pressures and compression of the inferior vena cava),
- increased systemic vascular resistance (afterload is increased secondary to compression of the aorta and systemic vasculature), and
- increased pulmonary vascular resistance (secondary to compression of the pulmonary parenchyma); and
- increased ICP in association with decreased cerebral perfusion
- (the increase in ICP is possibly secondary to decreased cerebral venous outflow – which is particularly concerning in this patient with pseudotumor cerebri, recent head injury, and an altered mental status.)
How is abdominal compartment syndrome diagnosed?
(A 7-year-old male presents to the trauma suite after falling from a height of eight feet when playing on a jungle gym. The child appears to have suffered some facial trauma, has a cervical collar in place, and is somnolent. His mother reports that he has a ventriculoperitoneal shunt to treat pseudotumor cerebri. There is no vascular access. Vital Signs: P = 139, R = 26, BP = 138/76 mmHg, O2 sat = 98% on non-rebreathing mask, T = 35.4 °C)
While abdominal pain and distention are commonly present (not always), dyspnea and reduced urine output are often the earliest signs of developing intra-abdominal hypertension.
Further evaluation of suspected abdominal compartment syndrome includes –
- abdominal computed tomography scanning (increased ratio of anteroposterior-to-transverse abdominal diameter, collapsed vena cava, bowel wall thickening, and bilateral inguinal herniation) and/or the
- measurement of the patient’s 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 mmHg are considered to be critical, but abdominal compartment syndrome may occur at pressures above 10 mmHg.
(*UBP Note – Recall that LIMB compartment syndrome is > 30 mmHg)
The triad of –
- elevated intra-abdominal pressures,
- significant abdominal distention, and
- evidence of end-organ dysfunction (i.e. renal, cardiac, and/or hepatic) strongly suggest the diagnosis.
The surgeon wants to proceed with surgery to relieve the abdominal compartment syndrome.
What preoperative workup would you require?
(A 7-year-old male presents to the trauma suite after falling from a height of eight feet when playing on a jungle gym. The child appears to have suffered some facial trauma, has a cervical collar in place, and is somnolent. His mother reports that he has a ventriculoperitoneal shunt to treat pseudotumor cerebri. There is no vascular access. Vital Signs: P = 139, R = 26, BP = 138/76 mmHg, O2 sat = 98% on non-rebreathing mask, T = 35.4 °C)
Recognizing that occult bleeding may be the cause of his condition, and that abdominal compartment syndrome can lead to electrolyte imbalances, fluid losses (third-spacing), and end-organ damage, I would begin by ordering –
- a 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:
- 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);
- ensure adequate muscle relaxation (abdominal muscle tone may contribute to increased abdominal compartment pressures);
- order a chest radiograph, to better evaluate the severity of any pulmonary compromise;
- order an echocardiogram to assess his cardiac contractility and volume status; and
- ensure that additional blood products, vasopressors, and inotropes were available in the operating room prior to induction.