CHILDHOOD TRAUMA

Trauma, accidental or intentional, is the leading cause of childhood deaths beyond infancy in developed countries responsible for ~40% deaths in pre-schoolers and ~70% deaths in school-goers or adolescents.

Epidemiology: Childhood trauma is relatively uncom­mon in infancy, with highest risk in 5-9 years age group. Boys are twice more commonly affected than girls. Maximum cases in India may be attributed to domestic accidents, e.g. accidental falls from a height, followed by vehicular accidents.

Evaluation of pediatric trauma depends on detailed history regarding mode of injury and thorough clinical examination, soon after initial ABC of resuscitation.

Following investigations are indicated in all cases of major trauma—(a) complete hemogram and blood grouping/cross-matching, (b) urinalysis for hematuria,

(c) biochemical evaluation with liver enzymes, renal parameters and electrolytes, (d) arterial blood gases, and (e) radiological evaluation with chest X-ray, relevant skeletal X-rays, USG and relevant CT studies.

Management: Mortality in trauma has a tri-modal distribution with ~50% deaths at the site of event, 30% within a few hours of hospitalizations and 20% after many days due to secondary complications. Conse­quently, immediate resuscitation is the most important component of trauma care.

General principles of management for a trauma victim are same as discussed previously under CPR (i.e. ABC of resuscitation), followed by revaluation and transfer to appropriate care center.

Pediatric trauma score (Table 27.20) is commonly used to decide the severity of trauma and need for PICU care. All cases with PTS lt; 8 indicate significant trauma and need referral to suitable trauma center. Further management depends on the type and severity of lesion.

One should never forget about medicolegal dimensions of childhood trauma, with due consideration to foul play and child-abuse.

Four major areas of concern in accidental trauma are—(a) head injury, (b) chest-wall injury, (c) abdominal injury, and (d) skeletal injuries and fractures.

TABLE 27.20: Pediatric trauma score

I. Cranio-cerebral trauma: Head injuries may be broadly divided into three categories—(a) superficial soft- tissue injuries of scalp, (b) skull fractures, and (c) brain injuries. Note that all, even severe, scalp/skull injuries are not necessarily associated with brain injuries. Conversely, serious brain injuries may develop without evidence of external injuries or skull fractures.

Superficial scalp injuries range from simple abrasions and lacerations to subgaleal/subperiosteal hematoma. As scalp wounds tend to bleed profusely, all major lacerations need suturing as soon as possible.

Skull fractures may be linear (single fracture line passing through entire thickness of skull), diastatic (gt;5 mm separation of sutures), depressed (an edge displaced posteriorly) and compound (with open skin surface).

Clinically, skull fractures may be asymptomatic or present with localized bogginess and pain. Important signs of basal skull fractures include—(a) periorbital blackness (Raccoon eyes), (b) petechial or subcutaneous hemorrhage on mastoid (Battle sign), (c) CSF leak from nose or ears (CSF rhinorrhea/otorrhea), and (d) cloudiness of tympanic membrane (hemotympanum).

Diagnosis depends on X-ray skull and CT scan, which is indicated in all head injuries with above mentioned signs of basal skull fractures.

Treatment: Linear, diastatic or minimally depressed fractures need no local treatment but indicate severe trauma and possibility of underlying brain injury. However, depressed fractures of gt;0.5 cm require surgical elevation and repair of underlying dura, if necessary. Compound fractures or penetrating skull injuries are surgical emergency, which need immediate debridement and prophylactic antibiotic therapy.

Brain injury after head trauma may be due to direct hit or counter-coup injury due to sudden movement of brain matter within the closed calvarium.

Younger children are more susceptible for severe brain injury than adults due to—(a) comparatively large head size, (b) open sutures/fontanels, allowing significant shift of brain matter after impact and large hematoma formation before clinical presentation, and (c) relative lack of supporting glial tissue.

Pathogenesis: Important pathogenic factors for brain injury after head trauma include:

• Immediate cerebral vasospasm and reactive neuronal swelling leading to hypoxic-ischemic insult,

• Vasogenic and cytogenic cerebral edema that usually begins after 12-24 hours due to impaired blood-brain barrier,

• Altered cerebral blood flow with intracerebral shunting, and

• Direct vascular injury with bleeding and local hema­toma, which may enlarge progressively due to further breakage of bridging vessels.

Types: Common types of neurological injuries after head trauma include:

a. Concussion, i.e.

Though general prognosis after concussion is good, a concussion lasting for gt;30 minutes or followed by focal neurological deficit on recovery indicates significant brain injury. Children with repeated concussion injuries due to abuse or contact sports are at risk for permanent brain damage.

b. Contusion or laceration injuries present with prol onged unconsciousness, raised intracranial pressure and focal neurological deficit. These injuries are usually caused by counter-coup mechanism (acceleration-deceleration injury), leading to more severe and diffuse axonal injury and cerebral edema. Early CT scan may be normal and any patient, whose neurological status does not correlate with CT findings, needs MRI that may reveal lesions in corpus callosum, internal capsule or rostral pons. Many cases die in acute phase unless treated intensively, while survivors may improve completely or with residual neurodeficit. Duration of coma after contusion is

directly related to mortality and sequelae.

c. Epidural hematoma is usually associated with linear, diastatic or depressed skull fractures due to tearing of middle meningeal artery or bridging veins. These cases typically present with lucid interval, i.e. immediate loss of consciousness followed by recovery for few minutes/hours before relapsing again to coma with progressive deterioration. Small epidural hematomas without neurological injury do not need evacuation but follow-up is necessary. Large collections compressing brain tissue or progressive neurological deterioration need surgical intervention.

d. Subdural hematoma may be acute or chronic. Acute subdural hematoma characteristically presents with progressive loss of consciousness and focal

neurological deficits, within few hours of injury.

Chronic subdural hematoma is commonest pre­sentation of intracranial hemorrhage in childhood, which may manifest after many weeks or months of injury with—(a) progressive head enlargement,

(b) seizures, (c) raised intracranial pressure, and

(d) anemia. Treatment includes subdural tapping, and some cases need repeated tapping or subdural shunt.

e. Subarachnoid hemorrhage is a common cause of post- traumatic hydrocephalus in children. Acute cases may present with signs of meningeal irritation. Treatment is supportive with variable prognosis.

f. Intracerebral hemorrhage is less likely to be traumatic in origin. Clinical presentation depends on the site and severity of hemorrhage, ranging from complete absence of symptoms to focal neurological deficits, seizures and coma, depending on the site of bleeding. Treatment is largely supp ortive with variable prognosis.

Diagnostic Evaluation of Head Injury

Evaluation of suspected head injury includes local examination for scalp injuries, underlying palpable fractures as well as neurological evaluation. Presence of any one of the clinical features enumerated in Table 27.21 indicates significant brain injury.

Headache, vomiting, excessive sleepiness or transient dizziness is common after head injuries and not by themselves of concern, if consciousness and neurological examination is normal. However, persistence of these symptoms beyond 24 hours needs further evaluation. Glasgow coma scale (GCS) is commonly used to monitor changes in neurological status of these cases (Table 18.7).

CT scan is the investigation of choice in all significant head injuries, which may reveal skull fractures, hematoma, cerebral edema or mass effect (mid-line shift). MRI is of little value in acute head injury except to detect very small lesions or diffuse axonal damage and usually reserved for later evaluation and follow-up. Similarly, X-ray skull is hardly informative except for fractures and may be avoided, if CT facility is available.

All cases of head injury should also be evaluated for cervical spine injuries, specially in presence of—

TABLE 27.21: Clinical indicators of brain injury

• Open head injury with exposed brain

• Depressed skull fracture gt;5 mm

• Progressive deterioration in consciousness

• Unequal pupillary size

• Seizures

• Asymmetric motor deficit

• Persistent otorrhea/rhinorrhea after head injury

• Persistent headache, vomiting, drowsiness gt;24 hours

(a) significant neck, back or limb pains on movements,

(b) acute flaccid para-/quadriplegia, and (c) sensory loss/paresthesia in limbs.

General Management of Head Injury

All patients with head injuries should be admitted or at least observed for a few hours before sending home with instructions to report back in case of any change in sensorium, persistent headache/vomiting, seizures or other neurological dysfunction.

Primary aim of the management in head injury after initial resuscitation is to control cerebral edema - the major cause of mortality and morbidity. All cases should be managed in head-up position. Continuous intracranial pressure (ICP) monitoring is indicated in all cases with severe head injury with an aim to maintain ICP lt;20 mm Hg and cerebral perfusion pressure gt;50 mm Hg, by:

• Correction of hypoxia and hypotension, which tend to exacerbate abnormalities in cerebral perfusion pressure. Mechanical ventilation is indicated in all cases with GCS lt;8. However, hyperventilation to maintain pCO₂ at 25-30 mm Hg should be used only in refractory ICP.

• Treatment of raised intracranial pressure: IV Mannitol (0.5-1.0 gm/kg) or 3% Hypertonic saline (IV 5-10 ml/ kg) in cases with signs of raised ICP, brain herniation, deteriorating sensorium or documented rise in ICP on monitoring, which may be repeated 6 hourly.

• Controlled fluid therapy with 2/3^rd maintenance as Ringer lactate or N/2 saline, due to risk of SIADH. Blood glucose tends to be higher immediately after head injury and dextrose-containing fluids should be restricted during early fluid therapy.

• Controlled sedation and muscle relaxation with barbi­turates, e.g. phenobarbitone, midazolam and/or vecuronium is useful to reduce cerebral edema and prevent seizures, as long as hypotension may be avoided. However, prophylactic anticonvulsants are not recommended.

• Treatment of fever is necessary to minimize metabolic brain requirements. Induced hypothermia has been used to control refractory rise in ICP, though clinical studies are inconclusive.

• CSF drainage via ventriculostomy is the first-line option for refractory rise in ICP, with/without other neurosurgical interventions, e.g. decompression craniotomy to evacuate mass hematoma. Other options include continuous barbiturate infusion (IV Pentobarbital 5-10 mg/kg over 30 min gt;1 mg/kg/hr) or controlled hypothermia (32-34°C) by surface cooling.

• Steroids are of controversial value in head injuries and should not be used routinely.

Outcome of head injuries in children is generally worse than in adults and depends on the severity of injury as well as quality of post-traumatic care. Post- traumatic epilepsy, hydrocephalus, meningitis and focal neurological sequelae are common among the survivors.

II. Chest wall injuries: Thoracic injuries may be caused by penetrating or blunt trauma, later being more common and often missed. Many chest wall injuries may also be due to resuscitative efforts.

Four major and life-threatening complications of chest­wall injury include—(a) flail chest due to rib fractures,

(b) tension pneumothroax, (c) massive hemothorax, and (d) cardiac tamponade due to hemopericardium.

Clinically, Inadequate response to appropriate cardio­pulmonary resuscitation may be the first sign of chest-wall injuries in children. Important indicators of chest-wall injuries include:

• Acute or progressive respiratory distress,

• Restricted/see-saw chest movements (flail chest)

• Surgical emphysema

• Distended neck veins

• Unresponsive hypotension or pulsus paradoxus

• Abnormal respiratory findings

• Muffled heart sounds, etc.

Management: All suspected chest wall injuries need immediate skiagram, and if necessary, diagnostic thoracocentesis to exclude pneumothorax, hemothorax or hemopericardium. Immediate needle aspiration of air/blood from pleural/pericardial space may be necessary in life-threatening emergency, followed by thoracic tube drainage or thoracotomy. Cases with massive hemothorax/hemopericardium should also receive blood transfusions.

III. Abdominal trauma: Blunt abdominal trauma is much more common in children than the penetrating injuries, with most frequently injured organs in descending order being—spleen, liver, genitourinary tract and intestines. Stomach, pancreas, biliary tree, and major vessels are usually injured only in penetrating injuries.

Splenic injury may be indicated by—(a) left shoulder pain that aggravates on pressure over Lt hypochondrium (Kehr sign), (b) persistent respiratory distress or vomiting,

(c) refractory shock due to continued blood loss, (d) peri-umblical blackening (Cullen sign). Diagnosis rests on USG/CT with/without radionucleotide scan.

Most cases are managed conservatively with intensive monitoring and transfusions. Surgical intervention with splenic repair/splenectomy is indicated in cases with—

(a) estimated blood loss of gt;40 ml/kg during 24-36 hours, (b) complete severance of spleen from its vascular supply, (c) fecal-contaminated hemoperitonium, or (d) co-existing head injury, where high volume circulatory support may be dangerous.

Liver injuries contribute to ~40% of deaths due to blunt abdominal trauma and 90% of them involve right lobe of liver.

Spectrum of these injuries, in order of increasing severity and decreasing frequency include - subcapsular hematoma, capsular tears, parenchymal lacerations, and burst injuries with vascular involvement.

Pain over right shoulder or hypochondrium is the most important warning signal of probable liver injury, which may be confirmed on USG/ CT scan. Management is largely conservative and surgical intervention is recommended only in life-threatening situation.

Renal injuries are frequently associated with other internal organ injuries. Pediatric kidney is more sus­ceptible for trauma due to relatively anterior loca­tion, compliant rib cage and immature abdominal musculature. Renal injury with trivial trauma indicates possible congenital malformation.

Important indicators of renal injury include—(a) hematuria with/without oliguria, and (b) renal angle pain/tenderness. Diagnosis rests on urine examination for hematuria, USG and CT with renal contrast.

Treatment is largely conservative and surgical inter­vention is indicated only in cases with—(a) refractory shock or continued fall in hemoglobin, and/or (b) clot- inducted urinary obstruction.

Intestinal injuries are almost always associated with other internal organ injuries and may present with—

(a) persistent abdominal pain and vomiting, (b) paralytic ileus, or (c) pneumoperitoneum. Immediate surgical intervention is indicated in these cases.

IV. Musculoskeletal trauma: While some musculoskeletal injuries are common in nearly all cases of trauma, presence of significant fractures or dislocations is indicated by—(a) severe localized pain/tenderness,

(b) deformity, and (c) restriction of movements with/ without other signs of inflammation.

Children are more susceptible for musculoskeletal injuries due to—(a) relatively more porous bones,

(b) developmental laxity of muscles/ligaments, and

(c) highly active lifestyle, which renders them prone for injuries, e.g. sport injuries.

Skeletal injuries may be broadly divided into:

(a) fractures, and (b) dislocations, e.g. pulled elbow, discussed in Chapter 23.8.

V. Superficial injuries (lacerations, abrasions and cuts): Lacerations are superficial skin tears due to blunt or shearing force, while cuts and stabs are caused by sharp objects. Abrasions are mere scrape of the skin due to friction against a hard surface. These injuries may be accidental or intentional and medico-legal consideration must be taken into account while managing them.

Management of these injuries involve—(a) local wound examination and management, (b) general supportive

measures including pain relief, and (c) exclusion of underlying deeper injuries.

All cuts and lacerations must be thoroughly examined for the size and depth of the wound, presence of any foreign body and associated vascular, neurologic, tendon, or other tissue injury. Initial goals of treatment are to establish hemostasis, minimize infection and restore skin integrity. Any significant bleeding must be controlled with external pressure or tourniquet. Skin flap, if any, must be returned to original position before application of pressure.

Subsequently, contaminated wounds must be irrigated with water or normal saline and dead tissues must be removed. Local wound care may need a topical anesthetic or regional nerve block before manipulation. Most superficial lacerations and cuts may be closed primarily with non-absorbable sutures, staples, skin adhesives or surgical tapes; followed by topical antimicrobial ointment and gauze dressing to prevent infection.

Prophylactic antibiotics are unnecessary and indicated only in open or grossly contaminated wounds or human/animal bites. Tetanus prophylaxis is indicated in unimmunized or partly immunized cases.

27.5.2