Neuroanesthesia Management in Pediatric with Traumatic Brain Injury in Emergency Operation
Fitri Hapsari Dewi
1, Achmed Rizal Fatahillah
11 Department of Anesthesiology and Intensive Therapy, Faculty of Medicine, Sebelas Maret University, Dr. Moewardi Regional General Hospital, Surakarta
INTRODUCTION
Pediatric neuroanesthesia is an exciting and challenging branch of anesthesia. Compared to adults, infants and pediatric's brains are more prone to injury and have different healing capacities. In pediatrics, physiological and neurological systems are still developed. In neonates, the cerebrospinal system and the blood-brain barrier are still immature, there is still maternal progesterone, and there are increased levels of endorphins.1–3 During neurologic surgery in pediatrics, careful control of cerebral perfusion should be exercised. Prolonged hypotension can lead to ischemic injury, while prolonged hypertension can lead to intraventricular hemorrhage and lifelong disability.3
The use of anesthetics in pediatrics also requires extra attention. In pediatrics, induction of anesthesia, both inhaled and intravenous, occurs more rapidly than in adults, owing to a more excellent ratio of alveolar ventilation to functional residual
capacity, a lower blood-gas coefficient of volatile anesthetics, and greater cardiac output.2 Potent volatile anesthetic agents and N-methyl-D-aspartate (NMDA) antagonists are associated with neuroapoptosis.3
The pediatrics airway is also anatomically different from the adult, making endotracheal intubation more difficult.
Pediatrics are also more susceptible to deoxygenation due to greater oxygen consumption.2
Currently, studies of pediatric neuroanesthesia have focused on patients' quality of life by reducing post-craniotomy pain and reducing postoperative neurocognitive morbidity.4 In tumor brain injury, paracetamol produces the lowest quality in pain reduction. However, it has minimal effect on nausea and vomiting.5
In this case, we report on the anesthetic management of a one-month-old male infant with acute on chronic subdural hemorrhage region in the frontotemporoparietal.
ABSTRACT
Background
:
One of the most exciting and challenging branches of anesthesia is to study pediatric neuroanaesthesia. The anatomy and physiology of the nervous system in pediatrics are still immature, so the management of pediatric neuroanaesthesia cannot be the same as adults. These managements include hemodynamic control, selection of anesthetic drugs used, and endotracheal intubation.Case: In this case report, we report a one-month-old male infant, weighing 4.6 kg, diagnosed with acute, chronic subdural hemorrhage (SDH) in the frontotemporoparietal region. Physical examination revealed a decrease in consciousness Glasgow coma scale (GCS) E2V2M5, with a pulse of 157 times per minute, a respiratory rate of 48 times per minute, and a 100% SpO2 with oxygen administration of 2 liters per minute through a nasal cannula. On airway examination, there was no gurgling, snoring, or hoarseness. The patient was planned for surgery with a general anesthetic endotracheal tube (GAET) with propofol 7 mg, fentanyl 5 µg, and rocuronium 2 mg. The patient received the analgesic paracetamol and fentanyl. The patient was hemodynamically stable during the 90-minute operation. The patient was admitted to the Pediatric intensive care unit (PICU) postoperatively.
Conclusion: Anesthesia treatment for traumatic brain injury in infants has unique problems that require knowledge of the anatomy and physiology of the pediatric brain.
Keywords: frontotemporoparietal region, neuroanaesthesia, paediatrics, traumatic brain injury Correspondence:
Dykall Naf’an Dzikri, MD*
Sebelas Maret University Ir. Sutami street No.36, Kentingan, Jebres, Surakarta City, Central Java 57126, Indonesia
e-mail:
Received: October 2021, Revised: December 2021, Published: January 2022
How to cite this article: Dewi, FH, AR Fatahillah. Neuroanesthesia Management in Pediatric with Traumatic Brain Injury in Emergency Operation.
Journal of Anaesthesia and Pain. 2022:3(1):5-9. doi: 10.21776/ub.jap.2022.003.01.02
Case Report
Journal of Anaesthesia and Pain, 2022, Volume: 3, No.1: 5-9 P-ISSN : 2722-3167https://jap.ub.ac.id E-ISSN : 2722-3205
CASE
One-month-old male pediatric, weighing 4.6 kg, was brought by his family to the hospital with complaints of unconsciousness, moaning, inactivity, and vomiting. There were no complaints of fever, convulsions, cough, runny nose, or shortness of breath. Previously, the patient was born spontaneously at the Public Health Center, assisted by a midwife.
On physical examination, showed Glasgow coma scale (GCS) E2V2M4 delirium, eyes open after receiving stimulation, verbal communication comes out in the form of a moan without words, and moving the body away from the source of pain when stimulated by pain. Symmetrical chest wall with a respiratory rate of 48 breaths per minute and 100% SpO2 with 2 liters per minute oxygen through a nasal cannula. Basic vesicular breath sounds were heard without additional breath sounds. The pulse is palpable regularly, 157 beats per minute.
End of extremity felt warm with capillary refill time (CRT) <2 seconds. Regular I-II heart sounds are heard. No heart sounds were heard. Pupils obtained isochoric 3 mm in diameter with positive light reflex right and left. No neurological deficit was found. Gurgling, snoring, and hoarseness was not found on airway examination. Mallampati and open mouth are difficult to evaluate. The neck can move freely.
On physical examination of the head, a prominent crown was found. The right and left conjunctiva looked anemic.
In the nose, a nasogastric tube (NGT) is attached. There is a little blackish-red product in the NGT. There were no abnormalities on physical examination of the mouth, ears, neck, thorax, abdomen, spine, or extremities.
On the follow-up examination on the day of hospital admission, the blood test showed a hemoglobin of 4.6 g/dl with a transfusion of 80 ml of packed red cells (PRC), a hematocrit of 13%, and an erythrocyte count of 1.4 million/µl of blood.
Meanwhile, the leukocyte and platelet counts were within normal limits.
On the first day of treatment, the hemoglobin level increased to 7.6 g/dl, the hematocrit to 21%, and the erythrocyte count to 2.6 million/µl blood. However, the leukocyte count increased to 19,900/µl. The hemostasis index of
the patient was prolonged, namely prothrombin time (PT) 25.3 seconds, and activated partial thromboplastin time (APTT) 50.1 seconds. On electrolyte examination, blood sodium is 128 mmol/l (hyponatremia), blood potassium is 6.1 mmol/I (hyperkalemia), blood chloride is 108 mmol/l, and blood calcium is 1.20 mmol/I. Furthermore, on the second treatment day, hemoglobin was increased to 10.3 g/dl, hematocrit to 28%, and erythrocyte count to 3.24 million/µl blood. Meanwhile, leukocytes returned to normal to 5,100/µl of blood.
On chest x-ray examination (18/12/20), the thymus was prominent, but there were no cast, pulmo, or abdomen abnormalities. Non-contrast head MSCT (18/12/20) showed acute on chronic subdural hemorrhage (SDH) in the bilateral frontotemporoparietal occipital region, posterior falx cerebri, bilateral tentorium cerebelli, and cerebral edema (Figure 1).
From the above description, the patient was diagnosed with decreased consciousness, vomiting, increased intracranial pressure, acute on chronic SDH in the frontotemporoparietal region, bleeding due to vitamin K deficiency, and suspected acquired prothrombin complex deficiency (APCD) with good nutrition. The patient was planned for surgery with a general anesthetic endotracheal tube (GAET) with propofol 7 mg, fentanyl 5 µg, and rocuronium 2 mg. This patient was managed by craniotomy for SDH evacuation. The American Society of Anesthesiologists (ASA) classification obtained ASA IV E, namely patients with severe systemic disorders that directly threaten their lives in emergency conditions. The patient was planning for surgery with GAET with propofol 7 mg, fentanyl 5 µg, and rocuronium 2 mg. The patient received the analgesic paracetamol and fentanyl.
Durante operation hemodynamics was relatively stable, hearth rate (HR) seen on echocardiogram (ECG) monitor ranged from 130–140 bpm, NIBP systolic was between 60–80 mmHg and diastolic was about 40–50 mmHg, monitors for heart and breath sounds through a precordial stethoscope were still attached, saturation was between 98% - 99%, bleeding during surgery is about 40 ml. The fluids were given by Ringer Fundin 40 ml and PRC 50 ml through an infusion pump, and the tube was warmed with a liquid warmer. The operation lasts approximately for 2 hours (Figure 2).
Figure 1. Plain head computed tomography (CT) scan and baby gram
Postoperatively, the patient was transferred to the Pediatric intensive care unit (PICU), still using the endotracheal tube (ETT) with the help of Jackson Reese ventilation. The first day of early postoperative: respiratory rate 30 breaths/minute, SpO2 100%, no additional breath sounds, blood pressure 80/55 mmHg, pulse rate 130 bpm, perfusion warm, consciousness can not be assessed, Hb: 13.2 gr/dl, Ht: 32, Leukocytes: 144.00/mm3, Platelets 253000/mm3, Na: 134, K: 4.2, Cl: 106. Therapy: head elevated 30 degrees, Ringer fundin infusion 14 ml/hour, antibiotics, anti-bleeding, fentanyl 0.5 µg/kg/hour, metamizole 75 mg/8 hourly. Six hours postoperatively: spontaneous breathing, 30 breaths, no additional sounds, blood pressure 80/50 mmHg, pulse 136 bpm, SpO2 99%, GCS: E3M4Vx planned extubation. The second day postoperative: respiratory rate 30 breaths/minute, SpO2 99%, no additional breath sounds, blood pressure 80/50 mmHg, pulse rate 140/minute, perfusion warm, no anemia, GCS E4M5V6 and planned to be moved to the room.
DISCUSSION
The main goal of anesthetic management in brain injury is to prevent secondary brain injury. Achieving this requires airway management of breathing, circulation, and control of increased intracranial pressure (ICP). The principle of neuroanesthesia can be abbreviated with the mnemonic ABCDE, namely; A= Airway must be free at all times. B= breathing includes controlled ventilation, PaCO, normocapnia in head injury, slightly hypocapnia in the tumor. PaO2 100-200 mmHg.
C= Circulation includes target normotension (avoid spikes in blood pressure) iso-osmolar fluid, normovolemia, normoglycemia, no disturbance of cerebral venous drainage/avoid increased cerebral venous pressure. D= Drugs by avoiding drugs and techniques that increase intracranial pressure and administering drugs that have a brain-protective effect. E= Environment by maintaining a hypothermic permissive temperature at the operation room (35°C) and in the ICU (35-36°C).6
Anatomical, physiological, and psychosocial differences in infants and pediatrics impact the handling of examination, diagnosis, use of tools, and drugs. It becomes a unique problem in pediatric neuroanesthesia. It contains little myelin, which
causes the nerve tissue to be easily damaged. In pediatrics, diffuse injury and brain edema are more common, so increased intracranial pressure is more likely to occur from a physiological and metabolic point of view: Cerebral metabolic rate of oxygen (CMRO2), cerebral blood flow, and cerebral autoregulation.
CMRO2 in pediatrics is 5.8 ml/100 g tissue/minute, higher than adults at 3.5 ml/100 g tissue/minute, while glucose requirements in pediatrics are 6.8 ml/100 g tissue/minute which is higher than the adult ratio. I.e., 5.5 ml/100 g tissue/minute, cerebral blood flow changes according to age in pediatrics 3 to 12 years. Cerebral blood flow 100 ml/100 g tissue/minute is higher than adults about 53 ml/100 g tissue/minute; from the above in pediatrics, the occurrence of ischemia and hyperemia of brain tissue is faster against CMRO2. Cerebral blood flow peaks between two and four years of age and persists at seven years. The range of brain autoregulation is also lower between 20-60 mmHg. This autoregulation is lost in critically ill infants, resulting in a linear relationship between CBF and blood pressure. In infants, the intracranial cavity is not as rigid as in adults because of fontanelles and sutures that are still open.
The increase in ICP by tumor-occupying lesions or cerebrospinal fluid obstruction is compensated by distension of the fontanelles and widening cranial sutures. However, a rapid rise in intracranial pressure cannot be compensated for due to bleeding and will lead to hypertensive intracranial pressure.1,7,8
In addition, there are also differences in the physiology of respiration and circulation in infants and pediatrics compared to adults. Regarding the differences mentioned above, the management of head trauma in infants and pediatrics must be followed/adjusted to the things mentioned above, both in the examination or treatment before, during, and after surgery. A computed tomography (CT) scan greatly assists preoperative assessment to assess the damage to brain tissue and signs of intracranial increase. The neurological evaluation for trauma uses the GCS scale. The assessment is the same for adults but modified as the Pediatric Glasgow coma scale (PGCS).7
In general, high ICP correlates with poor outcomes.
Still, ICP reduction measures and ICP monitoring in severe head trauma are less critical in infants because the fontanelles are not entirely closed. Some of the reasons for installing an ICP monitoring device are traumatic mass lesions and serial
80 70 67 65 62 64 70
74 76
45 40 43 42 46 48 50 47 43
135 130 136 138 139 140 139 136 135
35 33 34 34 33 32 33 32 34
100 100 100 100 100 100 100 100 100
0 20 40 60 80 100 120 140 160
0 8 . 3 0 0 8 . 4 5 0 9 . 0 0 0 9 . 1 5 0 9 . 3 0 0 9 . 4 5 1 0 . 0 0 1 0 . 1 5 1 0 . 3 0
Value
Time observation every 15 minutes
Systole Diastole HR EtCO2 SpO2
Figure 2. Intraoperative hemodynamic chart
neurologic examinations under the influence of sedation and muscle blockade. Monroe Kelly postulates that the head cavity is a rigid component, which includes the brain (80%), blood (10%), and liquor cerebrospinalis (LCS) (10%). In infants whose sutures have not closed can be seen from the stretching of the fontanelle or enlargement of the head. Chronic volume changes are generally compensated for, but not in rapid volume changes. The anterior fontanelle closes between 2–4 months, and the posterior fontanelle closes at 7–19.7 Airway management is very important in the early management of head trauma in infants, which is part of the ABCDE neuroanesthesia. The first evaluation is performed on the airway. There should be no airway obstruction because it will cause retention of CO2, resulting in hypercarbia and an increase in CBF. A decrease in PaO2 to below 50 mmHg will increase CBF drastically and worsen the patient's condition. Hyperventilation will only be given if herniation or neurological deterioration occurs.3 In this case, the patient's GCS is nine, and the airway is good; no intubation is required.7,9,10
In this case, breathing was still good; there were no additional breath sounds, respiratory obstruction, signs of respiratory failure, or use of respiratory support muscles. After traumatic brain injury, immediate oxygen intake will decrease 13%-27%. Therefore oxygen support is given through a mask 3- 4 liter/hour because prehospital hypoxia often worsens the patient's condition. Intubation and rescue breathing will be given if the GCS is < 8 (severe head injury) or signs of respiratory failure. Hypoxia should be avoided, monitored, and corrected quickly.8 Evaluation of fluids and electrolytes through blood pressure, heart rate, turgor, and urine volume is quite good; there are signs of mild-moderate dehydration considering this baby has been vomiting for two days.
Hypotension or dehydration should be corrected immediately in patients with eating disorders, inadequate intake, frequent vomiting, and loss of consciousness. Studies have shown that 18% of patients arrive at the emergency department hypotensive, with a mortality rate of 61%. Hypotension was diagnosed when the blood pressure was <5% of the mean blood pressure for that age.11 The choice of fluid in this patient is isotonic crystalloid, NaCl 0.9%.
Newfield believes that normal saline (NaCl 0.9%) is sufficient because trauma is often accompanied by increased blood sugar which increases the risk of neuronal damage.7 Some experts say it is permissible to use dextrose 5 % in fluids containing electrolytes, e.g., fluids containing D5 NS as much as 2–5 mg/kg/minutee.4 Although hypoglycemia is rare in pediatrics <1 year of age, it should be considered in pediatrics with prolonged fasting, mothers, Patients with a history of DM, low birth weight, hypopituitarism, adrenal insufficiency, pancreatic adenoma, and hepatoma. In the case of profuse bleeding, e.g., craniofacial reconstruction, tumors, it is advisable to install two intravenous lines.7,11 In this patient, the infusion is well established. If the infusion has not been installed, an infusion can be placed after the patient is anesthetized. Still, caution must be exercised in administering inhaled hyperventilation because it affects CBF and increases ICP.
Sedation was also not given because the patient had decreased consciousness. Sedation can be provided with close supervision, namely in patients with standard ICP, to control anxiety avoid hypertension and abnormal blood vessel rupture.
Osmotherapy with hypertonic saline (3% NaCl) mannitol 0.25-1 g/kg IV can be used cautiously to reduce
intracranial pressure. One of the side effects of osmotherapy is hypernatremia. Hypernatremia can be dangerous in neonates and infants whose kidneys are still immature. Thus, Cottrell argues that osmotherapy is given in severe brain injury if head- up and slight hyperventilation do not reduce cerebral edema.8,12
The temperature is maintained at 37 Celsius with a heating pad on the operating table. In traumatic brain injury, avoid an increase in temperature because an increase in temperature will increase CMRO2 and cause extensive neuronal damage. Although hypothermia can decrease CMRO2 in infants and pediatrics, it should still be considered due to the lack of research data.7 Standard monitors installed in these patients are precordial stethoscope, ECG, SaO2, EtCO2, non-invasive BP, temperature, urinary catheter. In cases of severe head injury with severe bleeding and the risk of rapid hemodynamic changes and neurologic deficits, additional monitors such as invasive BP, CVP, ECG, ICP, and SjO are needed.10
Anesthetic drugs are selected that have brain protection properties. In induction, the main goal is to control the airway and ICP by using propofol 2–2.5 mg/kg BW, atropine sulfate 0.02 mg/kg BW, fentanyl 1–2 ug/kg BW, rocuronium bromide as a relaxation facility for intubation, and maintenance of anesthesia, with oxygen, water, and sevoflurane. Although ketamine is commonly given for induction in infants and pediatrics, induction with ketamine can increase intracranial pressure because ketamine is not used in this case. N2O can increase the excitation and stimulation of cerebral metabolism in pediatrics because it is avoided, especially in the tight brain.
Sevoflurane has a minimal cerebral circulation effect, an insignificant increase in ICP compared to isoflurane, but the impact on perfusion pressure is better than isoflurane and desflurane. 7,10,12
Consideration of extubation in postoperative patients based on: uncomplicated operative procedure, normothermia at the end of the surgery, minimal hemodynamic changes during surgery, <6 hours of surgery, normovolemia and normotension, no coagulation abnormalities, no trauma and swelling in the face, neck and cavities mouth, not posterior fossa surgery, no cerebral edema, adequate preoperative consciousness.7
Postoperatively, he was not immediately extubated due to considerations of preoperative awareness (GCS 9) and the presence of cerebral edema. The patient was sent to the PICU, still intubated and on oxygen via Jackson Rees, and a saturation monitor was attached. Hemodynamics before transport stabilized. For postoperative sedation, rectal stesolid solution and analgesia with novalgin 50 mg/ 8 hours were given. Six hours in the PICU, the patient was fully awake and looked restless because of his ETT, stable hemodynamics, and adequate breathing, so extubation was performed. Care in the PICU with close monitoring; immediately re-intubate if there are signs of respiratory distress. The patient is put on mask ventilation of 3–4 l/minute. Observation on the second day hemodynamically stable, adequate breathing, warm perfusion, does not appear anemic, GCS E4M4V5, planned to move to the room.
CONCLUSION
The care of pediatrics with traumatic brain injuries is unique and complex. Good knowledge of a pediatric nervous system's anatomy and physiology is advantageous in understanding these problems.
ACKNOWLEDGMENT
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CONFLICT OF INTEREST None
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