© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023
S. T. Verghese (ed.)Anesthesia STAT! Acute Pediatric Emergencies in PACUhttps://doi.org/10.1007/978-3-031-24396-7_3

Somnolence After V-P Shunt Revision in an Infant

Nina Deutsch1  
(1)
Children’s National Hospital, Washington, DC, USA
 
 
Nina Deutsch
Keywords
Intraventricular hemorrhageVentriculoperitoneal shuntPostanesthetic somnolenceElectrolyte disturbancesAnesthesia for premature infants

1 Stem Case

A 13-month-old infant weighing 8 kg with a history of hydrocephalus is admitted to the postanesthesia care unit (PACU) after a revision of a ventriculoperitoneal (VP) shunt. She was admitted to the hospital the previous day secondary to altered mental status at home. Her mother reports that she vomited several times over the prior 24 h as well. Workup demonstrated that her shunt was no longer functioning properly.

Her past medical history is significant for birth at 27 weeks’ gestation via spontaneous vaginal delivery and very low birth weight. She had a grade III intraventricular hemorrhage (IVH) with subsequent hydrocephalus. She was diagnosed with a patent ductus arteriosus that required surgical closure at 1 month of age. She had bronchopulmonary dysplasia (BPD) for which she was intubated for approximately 4 weeks following birth. She was discharged home on oxygen, NG feeds, and apnea monitor. She also required sildenafil for elevated pulmonary pressures for the first 9 months of life. However, the apnea monitor has been discontinued, and she has had no oxygen requirements for the last 4 months. Her baseline CBC laboratory values demonstrated a hemoglobin of 10 g/dL and hematocrit of 31%.

She underwent initial VP shunt placement for her hydrocephalus at 3 months of age. She has been on NG feeds for 9 months and growing slowly. Her only medication currently is GE reflux medications and albuterol as needed.

Key Questions
  • What is an IVH and how is it graded?

  • What causes hydrocephalus following an IVH?

  • What is the treatment of hydrocephalus?

  • What are the anesthetic concerns of an infant with a history of prematurity?

  • What is the anesthetic management of an infant undergoing VP shunt revision?

Case continued: Her vital signs on arrival to the PACU are as follows: BP 74/38, HR 120/mt, sat 98%, and temp 36.3 °C.

Physical examination demonstrates a somnolent infant. She has a dressing in place on her head, and the fontanelle appears normal. She has poor muscle tone.
  • What are the signs and symptoms of VP shunt malfunction? How likely is it with her current presentation?

  • Apart from issues with the VP shunt, what are other potential causes of her somnolence?

Case continued: In reviewing the anesthetic, you note that the patient had a general anesthetic with an endotracheal tube. Sevoflurane, fentanyl (5 mcg), rocuronium, and acetaminophen have been administered. The rocuronium was reversed with glycopyrrolate and neostigmine and the patient was extubated awake per the anesthesiologist that did the case. She received a total of 80 cc of normal saline during the case and her blood loss was minimal. How does general anesthesia affect formerly premature infants in the recovery period?
  • What would be the most common presentation in the PACU if an excessive amount of opioid was administered to the infant? How would you treat this?

  • How would her presentation differ if inadequate reversal of the neuromuscular blocking agent was suspected? How would this scenario be treated?

Case continued: Further evaluation of the patient reveals that residual anesthetic agents are not the likely cause of the patient’s current presentation.
  • What are the other important diagnoses for somnolence to rule out immediately?

  • What tests or studies can help in the differential diagnosis?

Case continued: On physical exam, the patient responds to pain when stimulated; however, she is still difficult to arouse. She looks more lethargic with poor muscular tone. Her temperature has drifted down to 35.1 despite being swaddled up in blankets. An electrolyte panel and arterial blood gas are sent to the lab. Vital signs remain stable.
  • What findings on an arterial blood gas could result in the patient’s somnolence?

  • What electrolyte abnormalities could be the cause of her current condition?

  • If the patient’s electrolyte panel demonstrated hyponatremia, what would be the treatment? How should the treatment be carried out?

  • What are the concerns with treatment of hyponatremia?

Case continued: The laboratory study findings are as follows:

Test

Result

pH

7.34

pCO2

53

pO2

154

BE

−2

Sodium

142

Potassium

3.8

Glucose

40

Hemoglobin

9.9

Hematocrit

30

  • What are the implications of her hemoglobin and hematocrit values?

  • Which finding on the above labs is most likely the cause of the somnolence?

  • What is the treatment of this?

  • What treatment during the case could have helped to avoid this?

Case continued: The patient is administered 10% dextrose 2 mL/kg (16 mL) and has improvement in her mental status. She is now awake and crying. Vital signs remain normal. In review of the patient’s preoperative fluids and the anesthetic record, the patient received normal saline without dextrose from the time of her admission.
  • What maintenance fluids should she be given now?

  • If the laboratory values were all within normal limits (i.e., no electrolyte abnormalities), what would be the appropriate next step in the diagnosis and treatment of her somnolence?

  • At what point should neurosurgery be notified of the patient’s condition?

2 Discussion

2.1 What Is an IVH and How Is It Graded?

IVH is the leakage of blood into the cerebral ventricular space secondary to vascular fragility of the germinal matrix and changes in cerebral blood flow. Approximately 20% of preterm and very low birth weight (VLBW) newborns will develop an IVH, with more extensive bleeds more likely the smaller and more premature the infant. More than 50% of IVH will occur in the first 24 h after birth, while 90% will occur within the first week of life [1].

Diagnosis is made with the use of cranial ultrasound. The extent of the bleeding will determine the grade of IVH, as summarized in Table 1.
Table 1

Intraventricular grade based on ultrasound findings

Grade of IVH

Findings

I

Confined to the subependymal germinal matrix

II

Hemorrhage within the lateral ventricle without dilation and/or occupying less than 50% of the ventricle

III

Hemorrhage with distention resulting in ventricular dilation and/or hemorrhage occupying more than 50% of the ventricle

IV

Intraventricular hemorrhage that extends into the surrounding parenchyma

Clinical presentation of IVH can vary depending on the speed of onset of the bleeding. Acute neurologic deterioration will be seen with significant large, rapidly expanding IVH and is associated with poor outcomes. A slower IVH that evolves over hours to days will present as decreased alertness and activity, hypotonia, abnormal eye movements, and alterations in respiratory effort [1].

2.2 What Causes Hydrocephalus Following an IVH?

While the mechanism of posthemorrhagic hydrocephalus is not certain, it is thought that blood clots obstruct the flow of cerebrospinal fluid at the cerebral aqueduct or fourth ventricle outlets, resulting in obstructive hydrocephalus [2]. This is followed by a delayed communicating hydrocephalus secondary to abnormal cerebrospinal fluid absorption [1]. Ultimately, ventricular dilation can result in hypoxia, ischemia, decreased cerebral perfusion, increased development of free radicals, and destruction of the white matter [2].

2.3 What Is the Treatment of Hydrocephalus?

To prevent long-term sequelae of hydrocephalus, the definitive treatment is placement of a ventriculoperitoneal (VP) shunt. While this is the definitive treatment, it is typically not performed immediately secondary to the high risk of complications in very low birth weight infants, including skin ulceration, shunt malfunction, and the need for revisions. Often, temporizing measures such as lumbar punctures or external ventricular drains will allow for drainage of fluid and prevent significant dilation until the infant is older [1].

2.4 What Are the Anesthetic Concerns of an Infant with a History of Prematurity?

Babies born prior to 37 weeks’ gestation have an increased risk of developing several complications, the severity of which increases with lower gestational age at birth. These include but are not limited to the conditions listed in Table 2.
Table 2

Complications of prematurity

Complications of prematurity

Bronchopulmonary dysplasia (BPD)

Anemia of prematurity

Intraventricular hemorrhage

Patent ductus arteriosus (PDA)

Retinopathy of prematurity (ROP)

Neurologic abnormalities (cerebral palsy)

Multiple studies have demonstrated an increased risk for adverse events related to anesthesia or sedation for preterm children, children under 3 years of age, and those with significant comorbidities [3]. Furthermore, infants less than 60 weeks post-gestational age are at higher risk of developing postanesthesia apnea [4].

2.5 What Is the Anesthetic Management of an Infant Undergoing VP Shunt Revision?

Infants requiring VP shunt revision typically require a general anesthetic due to the need to potentially access the cranial and abdominal portions of the catheter. Most practitioners will elect to intubate the infant with an endotracheal tube to allow for control of ventilation and protection of the airway while the intra-abdominal portion of the procedure is done.

Revisions of the shunt can occur in the portion in the head, in the tubing between the head and the abdomen, or in the abdomen. If the entire shunt needs to be replaced, the tunneling of the new catheter is extremely stimulating and may require an opioid. If the patient otherwise meets extubation criteria at the end of the procedure, the infant is extubated to allow for a neurologic exam in the postoperative period.

2.6 What Are the Signs and Symptoms of VP Shunt Malfunction? How Likely Is It with Her Current Presentation?

VP shunt malfunction can present with an array of signs and symptoms. Bulging fontanelle, fluid collection along the shunt, depressed level of consciousness, irritability, abdominal pain, nausea and vomiting, and headache were found to be strongly associated with shunt failure [5]. Other signs of increased intracranial pressure, such as seizures, sunsetting eyes, and papilledema, can also be present. Fever is strongly associated with a shunt infection [5].

While this patient does have a common sign of shunt malfunction (depressed level of consciousness), she does not have a bulging fontanelle or vomiting in this postoperative period. While an issue with the shunt cannot be ruled out, other causes of her current presentation should be investigated as well.

2.7 Apart from Issues with the VP Shunt, What Are Other Potential Causes of Her Somnolence?

The differential diagnosis of delayed awakening following anesthesia can be divided into four main categories as outlined in Table 3 [6].
Table 3

The differential diagnosis of delayed awakening following anesthesia

Patient factors

Surgical and anesthetic factors

Extremes of age (former premature infant)

Long surgery and anesthetic

Gender

Muscle relaxant used

Genetic variation

Hypotension

Comorbidities (i.e., apnea of prematurity)

Hypoxia

Body habitus (i.e., obesity)

Embolism

Cognitive dysfunction

Cardiac/neurosurgery

Seizures

Regional techniques with sedation

Stroke

Painful stimulation

Drug factors

Metabolic factors

Dosage

Hypo-/hyperglycemia

Time of administration

Hypo-/hypernatremia

Blood-gas solubility

Hypothermia

Metabolism

Hypothyroidism

Excretion

Hepatic and/or renal failure

Drug interactions

Central anticholinergic syndrome

Fluid overload

Acidosis

Local anesthetic toxicity

Coagulation defects

It is imperative to confirm that the most life-threatening conditions, such as hypotension and hypoxia, are not present. Maintenance of the airway, breathing, and circulation are important for initial management. Once these are ruled out, a systematic review of the most common or likely issues should occur to begin appropriate therapy. In this scenario, the patient is maintaining her airway with normal vital signs. Therefore, other factors need to be evaluated promptly.

2.8 What Would Be the Most Common Presentation in the PACU if an Excessive Amount of Opioid Was Administered to the Infant? How Would You Treat This?

With the administration of opioids, it is imperative to monitor the patient for potentially harmful side effects. Excessive sedation has been shown to predict opioid-related respiratory depression and should be always monitored for while a pediatric patient is receiving opioid therapy [7]. Opioids also cause constriction of the pupils and can help in the differential diagnosis. Formerly premature infants such as this patient are at particular risk of apnea in the perioperative period [4]. Other known side effects of opioids include emesis, pruritis, ileus, and chest wall rigidity.

If excessive opioids are suspected, naloxone (0.1 mg/kg/dose) should be administered with titration to effect (i.e., reversal of sedation or respiratory depression). Support of the airway and ventilation should also be done to prevent excessive accumulation of carbon dioxide from the resulting hypoventilation that opioids induce. In this case she received 5 mcg of fentanyl at the time of surgical incision but no further opioids after the surgical procedure. Clinically significant dose variation can occur when drug volumes ≤0.5 mL are injected. Pediatric anesthesiologists must be aware of this possible unintended medication error when drawing small volumes of drugs to be administered to smaller patients [8].

Although the dose administered could have been more than intended unless drawn up in a small syringe and precise amount given, she was awakened and extubated fully awake at the end of the surgical procedure and then slowly became somnolent in PACU.

2.9 How Would Her Presentation Differ if Inadequate Reversal of the Neuromuscular Blocking Agent Was Suspected? How Would This Scenario Be Treated?

Inadequate reversal of a neuromuscular blocking agent will present with poor respiratory effort (shallow breathing or weak, rocking breaths), difficulty opening the eyes, and weakness of the extremities. The patient will also be difficult to arouse and not fully responsive to stimulation. Residual paralysis has been shown to increase the risk of passive regurgitation of gastric contents, worsen atelectasis, and interfere with hypoxic ventilatory control [9].

Train-of-four monitoring (TOF) is the standard to determine the presence of residual neuromuscular blockade. Importantly, a ratio of 0.9 is necessary to ensure the patient can protect their airway following extubation [9]. Despite this, in a recent survey of pediatric anesthesiologists, a minority of survey respondents always assess TOF, and the use of it was less in those who used sugammadex as their primary reversal agent [10].

If prolonged neuromuscular blockade is suspected, a reversal agent should be administered. The cholinesterase inhibitor neostigmine (0.07 mg/kg/dose) can be given with the anticholinesterase glycopyrrolate (0.01 mg/kg). However, it is inappropriate to administer these agents with the expectation of full reversal before at least T2 has been detected on the TOF. Alternatively, sugammadex, an agent that forms a 1:1 inclusion complex around steroidal neuromuscular blocking agent and thereby terminates its action (4–16 mg/kg), can be given despite the presence of a profound block [9].

2.10 What Are Other Important Diagnoses for Somnolence to Rule Out Immediately?

At this point, hemodynamic instability (hypotension, hypoxia, dysrhythmia) and side effects from the anesthetic and residual medications have been ruled out as potential causes of the patient’s somnolence. The patient’s temperature should also be taken to confirm that she does not have hypothermia, which can cause abnormal slowing of her metabolism and drug clearance. Since the patient’s temperature was normal on arrival to PACU, metabolic factors and underlying neurologic causes must now be taken into consideration.

Infants are at risk for developing hypothermia during transport and in recovery if warming measures are not taken to prevent it. Complications of perioperative hypothermia include coagulopathy and increased transfusion requirement, surgical site infection, delayed drug metabolism, prolonged recovery, and, in older patients, shivering and thermal discomfort [11].

2.11 What Tests or Studies Can Help in the Differential Diagnosis?

Electrolyte abnormalities can be determined with the use of point-of-care testing for sodium, potassium, and glucose levels. The presence of acidosis (either respiratory or metabolic) should also be investigated with analysis of an arterial blood gas (ABG). If these values are within normal limits, more rare but potential conditions such as renal and hepatic failure and hypothyroidism should then be considered.

2.12 What Findings on an Arterial Blood Gas Could Result in the Patient’s Somnolence?

Significant respiratory depression can result in hypercarbia. In preterm infants, the ventilatory response to carbon dioxide is significantly reduced. However, this improves with advancing age [12]. Elevations in carbon dioxide can result in somnolence if they are extremely high. Similarly, extreme hypoxia can decrease consciousness and should be evaluated as well.

2.13 What Electrolyte Abnormalities Could Be the Cause of Her Current Condition?

Abnormal levels of plasma sodium and glucose can cause significant somnolence. This can be determined with point-of-care testing or the analysis of a basic metabolic panel. A heel stick measurement of blood glucose is a rapid and readily available bedside test that can be performed as well.

2.14 If the Patient’s Electrolyte Panel Demonstrated Hyponatremia, What Would Be the Treatment? How Should the Treatment Be Carried Out?

Severe hyponatremia (less than 120 mEq/L) can result in cerebral edema, altered mental status, or coma [13]. This can be secondary to severe vomiting, medications such as diuretics, kidney or liver disease, syndrome of inappropriate antidiuretic hormone (SIADH), or iatrogenic causes, such as excessive administration of hypotonic intravenous fluids [14]. Once this has been determined, treatment should be undertaken.

In patients with severe symptoms such as vomiting, deep somnolence, seizures, coma, or cardiac arrest, 3% saline is administered to correct 4–6 mEq/L within 1–2 h, followed by a slower correction over the subsequent days to normal. Less severe clinical pictures should be corrected by 8 mEq/L/day or slower [13].

2.15 What Are the Concerns with Treatment of Hyponatremia?

Importantly, if correction of hyponatremia is too rapid, patients are at risk of central osmotic demyelination in which protein aggregation, DNA fragmentation, and programmed cell death lead to destruction of myelin. Evidence has shown that in patients with hyponatremia for less than 24 h, a more rapid correction is generally well tolerated compared to more chronic (greater than 48 h) hyponatremia [13].

2.16 What Are the Implications of Her Hemoglobin and Hematocrit Values?

The patient has a baseline hemoglobin and hematocrit that are indicative of anemia and could be a result of her poor feeding habits. The values that are obtained in the postoperative labs do not indicate that there has been significant perioperative bleeding. However, the presence of anemia in premature infants has been shown to be associated with an increased incidence of postoperative apnea compared to premature infants with a normal hematocrit [15]. This is less likely in this patient considering her age at the time of the procedure.

2.17 Which Finding on the Above Labs Is MOST Likely the Cause of the Somnolence?

Based on the reported laboratory values, the patient appears to have hypoglycemia. Age-based definitions of hypoglycemia in young children are presented in Table 4 [16].
Table 4

Age-based definitions of hypoglycemia in young children

Age

Plasma glucose level

Neonate <48 h old

<47 mg/dL

Neonates >48 h old, infants, and children unable to communicate

<50–70 mg/dL

Signs and symptoms of hypoglycemia include lethargy, change in level of consciousness, hypothermia, seizures, poor feeding, and hypotonia.

2.18 What Is the Treatment of This?

The patient should receive 200 mg of glucose per kg and 2 mL/kg dextrose 10% in water [D10W], intravenously.

2.19 What Treatment During the Case Could Have Helped to Avoid This?

Hyperglycemia can be seen in the perioperative period, prompting many anesthesiologists to infuse non-glucose-containing fluids such as normal saline or lactated Ringer’s solution intraoperatively. However, in this child, there are many risk factors for hypoglycemia. Riegger and colleagues studied the risk factors for intraoperative hypoglycemia in children and determined that these included young age, weight for age less than fifth percentile, ASA status greater than III, having a gastric or jejunal tube, poor feeding, and abdominal surgery [17].

This patient is an infant with a history of poor feeding and poor weight gain requiring gastric tube feeds. She also had recent vomiting associated with her shunt malfunction. These factors all put her at risk for having low glycogen stores and subsequent hypoglycemia. Therefore, monitoring of blood glucose is recommended either preoperatively with a heel stick glucose level, intraoperatively, or in the recovery room. Infusion of a glucose containing solution for maintenance fluids is indicated when hypoglycemia is likely.

2.20 What Maintenance Fluids Should She Be Given Now?

Postoperatively, a continuous infusion of glucose (D10W at 80–100 mL/kg per day) should be given with routine measurement of plasma glucose levels until the patient is taking fluids by mouth.

2.21 If the Laboratory Values Were All Within Normal Limits (i.e., No Electrolyte Abnormalities), What Would Be the Appropriate Next Step in the Diagnosis and Treatment of Her Somnolence?

If there were no electrolyte abnormalities found and the ABG was within normal limits, there should be an extremely low threshold to obtain a head CT scan. Considering her recent neurosurgical procedure, she is at increased risk of intracranial hemorrhage, stroke, or air embolus that warrants further evaluation. The possibility of subclinical seizures, potentially seen on an EEG, should also be considered.

2.22 At What Point Should Neurosurgery Be Notified of the Patient’s Condition?

Considering that this has occurred in the immediate postoperative period, the neurosurgeons should be notified earlier rather than later to discuss concerns related to the surgical procedure. Consultation with a neurologist to help guide further workup and management of the patient’s continued somnolence is important as well.

2.23 Where Should This Patient Be Monitored? And for How Long a Period?

The patient should be monitored overnight at the very minimum. She should be placed on a monitor that has pulse oximetry and EKG capabilities. Depending on the hospital’s monitoring capabilities on the inpatient floor, this can be done either there or in the intensive care unit if necessary.

2.24 What Would You Discuss with the Parents and the New Surgeons Who Are Going to Be Managing Her Overnight Stay and Discharge?

Postoperatively, a continuous infusion of glucose (D10W at 80–100 mL/kg per day) should be given with routine measurement of plasma glucose levels until the patient is taking fluids by mouth. Regular neurologic checks will be important as well to look for any clinical changes that would point to an issue with the new shunt.

3 Summary

Ex premature patients with GE reflux who are poor eaters, often seen to have low weight gain, have a high chance of developing hypoglycemia in the perioperative period. The history of vomiting in an infant with failure to thrive clinical scenario should alert the anesthesiologist of the possibility of perioperative hypoglycemia. If a blood glucose level is not done preoperatively, one should be checked intraoperatively, and appropriate therapy should be initiated.