The medical literature has detailed child abuse for over a century, from child slavery to battered children and shaken babies.
Since the 1970s evidence of specific inflicted injuries has been documented by radiologists such as John Caffey and pediatricians such as Henry Kempe in addition to multidisciplinary health care professionals. Their evidence has increased our understanding of the injuries sustained when babies are shaken, and they suffer abusive head trauma (AHT).
More than a decade ago Mary Clyde Pierce and her team introduced the TEN-4 bruising rule which has proved valuable in the identification of potential child abuse. Bruising in the body regions of the torso, ears and the neck in children less than four years may require further evaluation for child abuse (11). Inflicted injuries are not commonly associated with abdominal injuries. The incidence of hollow viscus injuries and mesenteric injury in all blunt abdominal trauma is less than 5 percent (8,9). They are a rare occurrence that can have devastating results (1,3). Abdominal injury should be considered with any child being assessed for non-accidental injury.
This article presents three children who sustained fatal abdominal injuries following blunt abdominal trauma.
Case No 1 – “Jack’s” Case*
Jack is a two-year-old male, who presented to the Emergency Department (ED) with an out of hospital cardiac arrest, he was the youngest of four siblings, with no medical history and an unknown immunisation history.
His parents phoned the Queensland Ambulance Service (QAS) when they found Jack unresponsive, in his bedroom, not breathing and with no pulse. His parent commenced cardiopulmonary resuscitation. There was an unclear downtime, but it was estimated to be 30 minutes before the paramedics arrived on the scene.
The QAS documented that Jack was apnoeic, asystolic, cool and mottled, with an unrecordable BP. They immediately took over CPR and administered a total of two doses of adrenaline plus a crystalloid bolus. He was intubated and ventilated and Jack was noted to have no gag reflex on intubation. They achieved return of spontaneous circulation (ROSC) after 20 mins with a weak central pulse, initially recorded as 44 beats per minute (bpm) which increased to 110 bpm. The patient then developed a sinus tachycardia. His GCS was 3 and his pupils were fixed and dilated.
The primary assessment and resuscitation took place immediately upon Jack’s arrival in ED. A rapid airway assessment revealed the endotracheal tube was in the correct position in the trachea and capnography was attached. The ETCO2 was recorded as 25mmHg, significantly lower than the normal range of 35-45mmHg. This acidosis was deemed to be indicative of his hypovolaemia and reflective of his poor perfusion. His ventilator respiratory rate was increased to 28bpm. Pulse oximetry was attached. A chest x-ray was ordered. Analgesia, sedation and paralysis infusions were prepared and commenced; his GCS remained 3/15.
Two 20-gauge intravenous cannulas were placed, and this enabled the administration of a warmed normal saline fluid bolus followed by an adrenaline infusion as well as sodium bicarbonate, cefotaxime, metronidazole and hypertonic saline infusion. Bloods were taken for venous blood gas including lactate, a full blood count, electrolyte and liver function tests, lipase, coagulation profile and a group and hold. Jack remained extremely hypotensive (47/29mmHg) and tachycardiac (156bpm) with a sluggish central capillary refill of approximately 4-5 seconds. Jack was critically unwell with circulatory failure.
In a heated resuscitation room, Jack was exposed when log rolled for inspection and examination of his posterior surfaces. He remained mottled both centrally and peripherally, with a core temperature of 32.6C.
He had extensive wounds to the back of both legs and on his buttocks. The wounds did not appear acute in nature, some of wounds were a brown-green colour, soiled with faeces and urine and had a malodorous faecal smell. They extended from his sacral area down the medial aspect of both his thighs and calves. There was redness and cellulitis of the surrounding skin consistent with infection. He was wrapped again in warm blankets.
A gastric tube was inserted to deflate his stomach, and a large amount of blood-stained fluid was aspirated from Jack’s moderately distended abdomen. A urine catheter was inserted, and the accurate volume of output used as a guide to his ongoing fluid resuscitation requirements.
Jack’s chest x-ray revealed evidence of free peritoneal gas in keeping with hollow organ perforation. Diffuse interstitial and air-space oedema were present. Jack had a positive FAST scan performed in the resuscitation bay, with free fluid noted in the abdomen. He was then transferred to medical imaging for a CT of his head, neck, chest, abdomen and pelvis with contrast. This showed free gas and fluid in the abdomen, consistent with perforated hollow viscus. The spleen and pancreas were intact. He was too unstable for definite surgery and an abdominal drain was inserted as a temporary measure to aid resuscitation.
He had a scalp bruise/haematoma of the forehead. His CT revealed early brain swelling but no intracranial haemorrhage or no fracture was identified. The various support lines and ET and NG tubes were appropriately positioned.
Jack progressively deteriorated despite maximum medical support including inotropes and antibiotics and he died that evening despite optimal clinical intervention.
A detailed history was taken from Jack’s parent surrounding the events of the evening and about the recency and circumstances of the infected wounds. Jack’s parent reported that they thought Jack had ‘hand foot and mouth’ disease from day care and they had treated his wounds with an antiseptic which was purchased from the pharmacy.
They had given Jack paracetamol when he cried out in pain.
His autopsy noted that some of the wounds were deep with the presence of bacterial infiltration.
He was noted to have 74 bruises mostly around his head and face, with 9 healing wounds some of which the postmortem indicated ‘could have been inflicted with the use of cigarettes’.
Jack had a fracture of his lower right incisor tooth with oral soft tissue swelling. He had pneumonia in his lungs with a secondary fungal infection.
At autopsy the internal examination noted the presence of air in the abdominal peritoneal cavity, a pneumo-peritoneum. A common cause of pneumo-peritoneum is a perforation of the bowel which may be induced by blunt trauma. His autopsy revealed that he had fibrinous adhesions involving his small intestine, inflammation around the porta hepatis in his liver and a perforation in the second part of his duodenum (D2).
Jack had a focal area of infarction demonstrating tissue death due to inadequate blood supply to his right kidney.
Ultimately, Jack’s cause of death was overwhelming sepsis from his untreated infected wounds and or from his perforated duodenum. Porta hepatis injuries from blunt trauma are extremely rare and are usually associated with rapid deceleration or torsion that accompanies high speed mechanisms of injury (12).
Case No 2 – “Olivia”*
A 000-call for a 23-month-old Olivia reported that this child was unresponsive, an out of hospital cardiac arrest. The child had no known past medical history and an unknown immunisation status.
On assessment the paramedics noted her stomach was swollen and her lips were dark purple. There was dried vomit on her face. Her eyes were open, and her pupils fixed. Although it was winter, the child was wearing a thin singlet and she had a soiled nappy with dried melena noted. Olivia was unconscious with a GCS of 3/15.
Olivia was intubated and ventilated at the scene and on route to the ED she had no palpable pulse despite CPR being delivered by the paramedics. CPR and rounds of adrenaline were given every four minutes, in addition to two intravenous fluid boluses.
After forty minutes of continuous CPR with no ROSC, resuscitation efforts were ceased, and Olivia was pronounced dead.
At autopsy Olivia’s external body examination revealed a total of 46 separate bruises to her body, two on her head, twelve on her trunk, four on her buttocks, one on her forearm, eighteen on her left leg and nine on her right leg. She had a contusion on her neck.
She had healing fractures to her lower extremities, some of these were noted to have been caused by ‘moderate or severe force’.
Her abdomen was swollen, and her autopsy revealed severe injuries to her abdominal and pelvic cavity with a tear of her small bowel. She had a 10mm full thickness perforation in the third part of her duodenum (D3) that was noted to be necrotic. There were haemorrhages within the soft tissue posterior to her duodenum and within the pancreatic tissue.
The autopsy concluded that Olivia’s cause of death was abdominal injuries, and the blunt abdominal injury resulted in bacterial contents leaking from Olivia’s bowel into the adjacent abdominal cavity resulting in bacterial peritonitis. The infection progressed to the child’s blood stream leading to sepsis that led to her death. It could not be determined if this blunt force was caused by a single blow (squeeze, kick, impact with a blunt instrument) or by separate repeated incidents of trauma.
Case No 3 – “Rory”*
Rory was an eighteen-month-old boy that presented to ED following a scald injury. His caregiver reported that the hot tap in the bath had been accidently turned on, and as a consequence Rory sustained scald injuries to a large proportion of his body.
Queensland Ambulance Service (QAS) initiated the cool running water for 20 minutes on route to hospital. He had no known past medical history. Immunisations were up to date.
Rory’s management in ED included; intubation and ventilation for anticipated massive fluids shifts, analgesia and ongoing ventilation requirements.
A nasogastric tube was inserted to deflate a mildly distended abdomen. IV access was obtained through his left jugular vein and his right femoral vein, and after two fluid boluses were given, the parkland formula was used to calculate the burns replacement fluids in addition to maintenance fluids. There was difficulty initially inserting a urine catheter due to swelling of his foreskin, but once successful, his fluids were titrated to his urine output of one millilitre per kilogram per hour. Morphine, midazolam and vecuronium infusions were commenced. His GCS remained 3/15.
Rory’s burns had a clearly demarcated line between burnt skin and undamaged skin, with no splash marks consistent with a child being immersed in scalding water. Laser doppler of Rory’s hands and feet indicated deep partial thickness to full thickness burns. Rory also had circumferential burns with decreased perfusion to his lower limbs and upper limbs. He went to the operating room for tissue release with escharotomies of his ankles, feet, hands and fingers and left thumb.
At the time of his escharotomy, Rory’s abdomen was noted to be more distended and an abdominal x-ray and CT scan was requested. The degree of distention was unusual for a burn injury, more than one would expect with a recognised complication of large burns — paralytic Ileus.
He remained tachycardiac (190bpm) and in spite of the increasing respiratory support, continued fluid resuscitation, cardiovascular stabilization, pain control, and burns management he continued to deteriorate. His CT indicated small bilateral pleural effusions, marked ascites, pneumatosis of the gastric wall and a pocket of free gas. His abdominal x-ray indicated an increase amount of free air in peritoneal cavity.
Rory had fresh blood noted in his mouth and blood-stained urine, coffee ground nasogastric aspirates.
The decision was taken to perform a surgical exploratory laparotomy in theatre. In the operating room it was discovered he had copious malodorous free gas and dark blood-stained intraperitoneal fluid. Rory had ischemic perforation of the greater curve of the stomach, with local soiling of the gastric contents. His spleen was infarcted (black and hard). His stomach and duodenum were gangrenous with no peristalsis. The colon was extensively infarcted (foregut and midgut) and gangrenous to his rectum. He had multiple tears and hematomas in the base of his midgut mesentery suggesting ‘a shearing or distraction’ injury. His bowel was completely devascularised. His kidneys were swollen and blanched.
Rory’s abdominal injuries were nonsurvivable.
Rory’s autopsy detailed his burns, as being 60 per cent TBSA in keeping with the surgeon’s calculation. The appearance of these burns was suggestive of ‘partial submersion in a prone position’.
There was also evidence of trauma to the head, with both bruising on the forehead and frontal scalp and a small subdural haemorrhage.
There were ‘no complications of the surgical procedures.’ The small bowel showed patchy serosal congestion, with a 20mm contusion in its mid region. The mesentery showed several small lacerations which were greatest around the mesenteric root. The liver and spleen had changes suggestive of ischaemic injury. The lining of the abdominal cavity (peritoneum) was congested and the peritoneal cavity contained blood-stained fluid. The stomach was perforated and there were tears in the mesentery.
It was deemed that Rorys cause of death was a combination of hypovolemia and sepsis, with extensive ‘damage to the gastrointestinal tract’ which resulted from impaired blood supply (ischaemia) and a devascularised bowel. The changes in the stomach and bowels were of a variable degree but it was most severe in the stomach which had perforated.
A possible cause proposed for these injuries was ‘blunt force trauma’ to the abdominal wall.
Young children (particularly those under four years of age) who present with an acute abdomen, with an unclear mechanism of injury should have inflicted injury (physical and sexual abuse) included as a differential diagnosis.
The caregivers of abused children do not always seek timely medical attention; therefore, it is imperative that if a child presents for medical attention that clinicians are cognisant of the signs and symptoms of inflicted trauma.
In Queensland registered medical officers and registered nurses are mandated to make a report to the child safety statutory authority, now called the Department of Child Safety, Youth, Justice and Multicultural Affairs (DCYJMA) if they suspect maltreatment. The aim is risk mitigation and protection of these vulnerable children.
In addition, a comprehensive assessment of the child should be undertaken, including a detailed history and an extensive clinical examination. Bloods extracted and analysed include hepatic enzymes (amylase and lipase) with clotting disorders and metabolic disorders ruled out. A urine specimen should be reviewed for toxicology with a drug screen performed in the laboratory. An ophthalmology referral will enable a retinal exam to detect the presence or absence of retinal haemorrhages, and ocular imaging to be captured. A skeletal survey may be undertaken and repeated after two weeks to detect any new periosteal bone.
Bone scans using radioactive tracers offer greater sensitivity to detect a bone injury that may not be seen on a standard xray. A CT scan of the head should be conducted to assess blood and bone injury particularly in the setting of abusive head trauma. In addition, a contrast enhanced CT of abdomen is the ‘gold standard’ to determine small bowel or duodenal injuries. A magnetic resonance imaging (MRI) scan is usually undertaken to assess more detailed soft tissue and organ injury.
The TEN-4 clinical decision rule can be used if it aids the identification of potential child abuse and guides onward child protection consultations. Patterns of burn injuries should be referred to burns specialists for their expert opinion on accidental or inflicted thermal injuries.
Mortality rates for critically injured children have decreased substantially in the last twenty years as trauma teams have streamlined their approach to diagnosis, prompt intervention and management. These inflicted abdominal injuries tragically led to the untimely death of Jack, Olivia and Rory who suffered gastrointestinal perforations with peritonitis and septicaemia and in Rory’s case an infarcted devascularised gut.
All three cases were complicated by a delayed presentation for medical treatment. Charges of child cruelty or manslaughter for the perpetrators, and bystander witnesses, is a matter for the justice system.
* Names and some specific details have been changed or omitted deliberately, to better de-identify these children.
Tona Gillen is nurse manager, trauma, at Queensland Children’s Hospital.
- Interchangeable terminology - Intentional inflicted injuries, child slavery, child abuse, physical abuse, battered children, shaken babies, suspected child abuse and neglect, non-accidental injury.
- Abusive Abdominal and Thoracic Trauma
Sandra Herr et al, Clinical Paediatric Emergency Medicine, 2006
- A review of children with severe trauma admitted to paediatric intensive care in Queensland, Australia. M Couthard et al . PLOS one, 2019
- A systematic review of abusive visceral injuries in childhood—Their range and recognition
S.A Maguire et al, Child Abuse & Neglect, 2013
- Duodenal perforation: An interesting case report. Kirsten J Donald et al, Emergency Medicine Australasia, 2005
- Focused Assessment with Sonography for Trauma. Benjamin A. Bloom et al, 2020
- Gastrointestinal Perforation and the Acute Abdomen. John T Langell, Medical Clinics of North America, 2008
- Gastrointestinal perforation: clinical and MDCT clues for identification of aetiology. Styliani Pouli et al, 2020
- Hollow viscus injury due to blunt trauma: A review
T.Bège et al, Journal of Visceral Surgery, 2016
- Incidence of hollow viscus injury in blunt trauma: an analysis from 275,557 trauma admissions from the East multi-institutional trial
Dorraine D Watts et al. Journal of Trauma 2003
- Mandatory reporting laws. In A. Hayes & D. Higgins (Eds.), Families, policy and the law: Selected essays on contemporary issues for Australia. Mathews, B. et al, 2014
- Pediatrics. Bruising Characteristics Discriminating Physical Child Abuse from Accidental Trauma. Mary Clyde Pierce et al. 2009
- The range of visceral manifestations of non-accidental injury. CS Ng et al. 1997
- Traumatic injuries to the porta hepatis case report and review of the literature. P Thenunis et all. Injury 1989.
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