Iatrogenic and Traumatic Injuries
Cynthia B. Jensen, Sheila S. Galbraith
Introduction
A variety of untoward events may befall the developing infant while in utero or postpartum. Some of these perinatal problems are inherent in the birth process. Others are related to technologic advances that have become standard obstetric and nursery practice. Although these diagnostic and therapeutic procedures have reduced morbidity and mortality, some also pose a significant risk for iatrogenic complications. Sequelae of iatrogenic complications can also present later in infancy or early childhood. Moreover, iatrogenic and traumatic injuries can occur in older infants. This chapter emphasizes those occurring in neonates and young infants. More extensive discussions of non-accidental injury (more common in older infants) can be found in other textbooks.
Puncture wounds
Amniocentesis
Amniocentesis is currently the most widely used technique for the antenatal diagnosis of genetic disorders. Although routinely a second-trimester procedure, it may also be performed in the third trimester for management of isoimmunization or evaluation of fetal maturity, or late in the first trimester for fetal karyotyping and DNA analysis.1 The risk of damage to the fetus is quite low, particularly in the middle trimester; nevertheless, needle puncture of the skin and sometimes of the underlying structures is a possible complication. Estimates of the incidence of cutaneous scarring ranged as high as 9% in the 1970s; however, with increased experience and the advent of real-time ultrasonography, this figure has dropped to less than 1%.2 Despite the benignity of the procedure, the incidence of fetal injury rises dramatically with an increasing number of needle passages at amniocentesis.
Amniocentesis scars are depressed, dimple-like lesions that usually measure 1–5 mm in diameter, although scars as large as 12 mm in diameter and 8 mm in depth have been documented (Fig. 8.1). They may be solitary or multiple, and are often inconspicuous. Shallow linear lesions have also been described.2 Although sometimes present at birth, they are often not noticed until the infant is several weeks to months old. The most frequent sites of injury are the extremities, followed by the head, neck, and chest. Mid-trimester amniocentesis has the lowest risk of puncture because the fetus occupies only about 50% of the amniotic cavity; in both the first and third trimesters, there is less room to maneuver, and sudden movements of the fetus may make injury unavoidable.
Amniocentesis scars must be differentiated from congenital sinus tracts, aplasia cutis, focal dermal dysplasia, amniotic band syndrome, accessory nipples, and dimples associated with congenital rubella, diastematomyelia, Bloom syndrome, and cerebrohepatorenal syndrome.
Chorionic villus sampling
Chorionic villus sampling (CVS), which can be performed early in the first trimester, is the preferred procedure for patients at risk for certain single gene disorders. The technique yields mitotically active cells suitable for rapid DNA analysis and permits detection of placental mosaicism. Of concern, however, are reports of increased risk of limb and jaw malformations as well as an increased risk of infantile hemangiomas, particularly in fetuses undergoing CVS at <9 weeks’ gestation.1,3 An analysis of 138 996 outcomes in a multicenter study disputes this notion4 but is not universally accepted, and thus the issue remains a controversial area still under study. A distinctive defect of absent distal third fingers with tapering of other digits, was more recently reported to be associated with exposure to CVS in a review by Golden and colleagues.5
Fetal monitoring
Intrauterine electronic monitoring of the fetal heart rate via a spiral electrode attached to the presenting part has become standard obstetric practice. Complications are infrequent and consist mainly of minor lacerations, ulcerations, scalp abscesses, and herpetic infections.6,7 Herpetic infections are extremely rare; however, incidence figures for scalp abscesses in monitored infants due to other agents, range from 0.1% to 5.4%,8,9 with most in the 0.3–0.5% range.
Scalp abscesses are localized collections of suppurative material that present as erythematous, indurated masses with or without fluctuance in the area of electrode application. Usually solitary, they vary in size from one to several centimeters. Onset can be as early as the first day or as late as the third week, but they are most frequently noted on the third or fourth day of life. Enlarged posterior cervical lymph nodes often accompany the abscess. Usually the inflammation remains confined to the skin; however, in a review of neonatal scalp abscesses by Weiner and coworkers, reported complications can include osteomyelitis, cellulitis, seizures, meningitis, brain abscess, bacteremia, and death.10 Contributing factors in some series (but not others) appear to be high-risk pregnancy (prematurity), prolonged rupture of the membranes, and long duration of fetal heart rate monitoring. The presence of amnionitis6,8,11 does not seem to be correlated. Although an infectious cause has been disputed – because cultures obtained from some infants have been sterile – data from large series support the concept of an infectious etiology. Okada and colleagues8 reported on 42 infants with scalp abscess, 100% of whom had positive cultures: 85% were polymicrobial, 58% grew both aerobes and anaerobes, 33% grew aerobes only, and 9% grew anaerobes only. The predominant aerobic organisms were Staphylococcus epidermidis and Streptococcus groups A and B; the predominant anaerobes were Streptococcus and Peptococcus. A confirmatory study by Brook and Frazier12 demonstrated similar findings in 23 infants. Andrews and colleagues evaluated vaginal cultures from 5732 mothers and found the MRSA colonization rate to be 3.5%, with no cases of early-onset neonatal MRSA infection postpartum.13 It is critical to distinguish infants with intrapartum inoculation of herpes simplex virus (HSV) from neonates with a bacterial scalp abscess (see Chapter 13). Although HSV infection as a complication of scalp monitoring is distinctly uncommon, the outcome can be devastating, with permanent neurologic damage,14 or death from systemic disease.15 Both type 1,15 and type 2 infections7 have been documented; unfortunately, this complication may occur with asymptomatic shedding of the virus and in the absence of a history of overt clinical disease.
Scalp abscesses usually heal uneventfully but may leave minor degrees of scarring, hypopigmentation, and alopecia, causing confusion with aplasia cutis, nevus sebaceus, or focal dermal hypoplasia in later years.
Needle marks and scars
Needle marks consisting of hypopigmented pinhead-size lesions, when presenting in large numbers, may impart a speckled appearance to the skin. These marks are due to venipuncture, arterial punctures, and catheter insertion, and are most commonly seen on the scalp, hands, wrists, feet, ankles, arms, and legs. Fox and Rutter16 reported an improvement in the appearance of needle marks by 9 years of age, in their cohort of 90 patients. Heel-pricks from blood sampling may cause dimpling or, rarely, calcified nodules (see below), hypertrophic scars, or even gangrene (Fig. 8.2).
Birth-related trauma to the skin and scalp
Injury to the soft tissues may occur in the setting of a prolonged labor because of cephalopelvic disproportion (Fig. 8.3), or with forceps delivery. Erythema, abrasions, and forceps marks are most common over the face, but rarely cause significant injury, and usually resolve spontaneously (Fig. 8.4).
Petechiae and ecchymoses
Petechiae on the head, neck, and upper body are likely to be caused by pressure differences that occur during passage of the chest through the birth canal. It is important to exclude the possibility of an underlying infection or hematologic disorder with appropriate laboratory studies. Petechiae caused by trauma are innocuous and usually fade within 2–3 days.
Ecchymoses may be extensive following a traumatic or breech delivery. Large areas of bruising may result in hyperbilirubinemia, requiring phototherapy. Ecchymoses resolve gradually, but may take up to several days to disappear completely.
Caput succedaneum
Diffuse edematous swelling of the scalp, when it is the presenting part, is known as caput succedaneum. Extravasation of blood or serum above the periosteum occurs as a result of venous congestion caused by pressure of the uterus, cervix, and the vaginal wall on the infant’s head during a prolonged or difficult labor and delivery. Because the accumulation of fluid is external to the periosteum, it crosses the midline and is not limited by the suture lines. If labor is prolonged, petechiae, purpura, and ecchymoses, as well as molding of the head and overriding sutures, may be prominent features. Unlike cephalhematoma, with which a caput is occasionally confused, the skin findings resolve within a few days. The molding may take a few weeks to disappear. Occasionally, if severe, tissue necrosis and a localized area of scarring alopecia may ensue.
Cephalhematoma
Cephalhematoma is caused by rupture of the emissary or diploic veins of the skull during a prolonged or difficult labor or delivery. The result of subperiosteal hemorrhage, it differs clinically from caput succedaneum in that it is almost always unilateral. The hematoma is localized most often to the area over the parietal bone, and the mass is confined by the periosteum, which adheres to the margin of the bone (Fig. 8.5). Cephalhematoma less frequently involves the occipital bones, and only rarely the frontal bones. If both parietal bones are involved, the hematomas are sharply demarcated and separated by a midline depression corresponding to the intervening suture. The overlying scalp is not discolored.
Cephalhematomas are seen more commonly in vacuum-assisted vaginal deliveries than in forceps or spontaneous births.17,18 The swelling may not become apparent until several hours to days after birth. As the hematoma ages, it develops a calcified rim and is gradually completely overlaid with bone. Estimates of underlying skull fractures have ranged from 5.4% to 25%.19 Differential diagnosis includes caput succedaneum and cranial meningocele.20 Meningoceles can be differentiated by the presence of pulsations, increased pressure when crying, and the presence of a bony defect on X-rays. Infection of the mass and severe hemorrhage resulting in anemia and hyperbilirubinemia are rare complications for which antibiotics, blood transfusions, and phototherapy may be required.21 Treatment is unnecessary for uncomplicated lesions. Most cephalhematomas are resorbed during the first few weeks of life and are of no consequence.17 Occasionally, they calcify and persist for months to years.
Subgaleal hemorrhage
Subgaleal hemorrhage is a rare but potentially life-threatening complication that occurs when emissary veins are ruptured, most commonly by instrumentation at delivery. Like cephalhematomas, vacuum-assisted delivery increases the incidence of subgaleal hemorrhage. Bleeding into the loose connective tissue of the subgaleal (also known as the subaponeurotic) space can be extensive, leading to severe anemia, disseminated intravascular coagulation (DIC) and hypovolemic shock.22 The area of swelling crosses suture lines and can extend from the brow line to the nape, as well as laterally to the temporal fascia located behind the ears.23 Unlike cephalhematomas, which are limited by the periosteum and suture lines, the aponeurotic space may accommodate up to 260 mL of blood, approaching the circulating blood volume of a neonate, which is approximately 80 mL/kg. Physical assessment may reveal dependent swelling on the scalp that varies from firm to fluctuant, and fluid waves may be present when the area is palpated. The neonate may exhibit hypotonia, pallor and tachypnea. As hypovolemia worsens, signs of poor perfusion, tachycardia, oliguria, and eventually hypotension may ensue. The infant must be closely monitored for signs and symptoms of neurologic compromise, shock and bleeding. Treatment is aimed at maintaining normovolemia, and controlling coagulopathy.
Untoward effects of vacuum extraction
The formation of some type of hematoma is a common occurrence with the use of a vacuum extractor, although with the introduction of softer silicone cups, the risk has been reduced.24 A ‘chignon,’ or artificial caput succedaneum, is created by adherence of the cup to the scalp and is most obvious immediately following removal of the cup. However, the swelling usually disperses relatively rapidly after birth. If a chignon is formed in the presence of a natural caput, the scalp may have a boggy sensation suggesting subgaleal hemorrhage (see above).25
Cephalhematomas, a ring of suction blisters, lacerations, and abrasions may also result from the use of the vacuum extractor.26 The latter are usually the result of prolonged traction and sudden detachment of the cup. Subcutaneous emphysema of the scalp has been attributed to vacuum extraction in an infant with a coexistent scalp electrode wound.27
Cases of vesicular eruptions following vacuum extraction with or without the presence of herpes simplex virus (Fig. 8.6) have been reported, presumably from the combination of mechanical trauma and colonization.28
Halo scalp ring
Alopecia in an annular configuration, presumably the consequence of localized injury during the birth process, has been referred to as ‘halo scalp ring’ injury.29 Often – but not always – there is a history of a prolonged labor. The hair loss is manifest at birth, or shortly thereafter, as a band of alopecia ranging in width from 1 to 4 cm, usually located over the vertex (Fig. 8.7A). There is typically an associated caput succedaneum and in some instances, frank tissue necrosis (Fig. 8.7B). If the injury is mild, the alopecia is usually temporary;29,30 however, scarring alopecia may result if the injury is severe (Fig. 8.7C).31,32 The areas of scarring can often be corrected with plastic surgery. The presence of halo scalp ring implies soft-tissue hypoxia and as such, infants with this condition should be monitored for developmental defects, which could have accompanied prolonged labor and associated hypoxic states.
Lacerations
Scalpel lacerations to the infant during cesarean section represent a potential form of injury. Smith and coworkers33 found an incidence of fetal injury of 1.9% in a series of 896 cesarean deliveries. Lacerations were much more common in those deliveries where the indication was nonvertex presentation (breech or transverse lie). In these infants, the injuries were almost always located on the lower portion of the body, whereas infants in a vertex presentation usually sustained their lacerations on the head. Failure to recognize the injury in the delivery room was a common occurrence.
Burns and thermal injury
Chemical burns
Very low birthweight (VLBW), preterm infants are particularly predisposed to skin damage from topically applied chemicals and medications.34 This is largely due to an immature epidermal barrier, and their vulnerability may be accentuated by hypoxia and hypothermia.
Chemical burns from concentrated disinfectants or other solvents have been reported following their use in the neonatal intensive care nursery (see Chapter 5). Burns are evident as intense erythema associated with blister formation and sloughing of the damaged skin (Fig. 8.8).
Isopropyl alcohol has caused second- and third-degree burns when substituted for electrode paste beneath electrocardiograph (ECG) leads or used as a preparation for the umbilical area. Alcohol-based skin cleansers, containing chlorhexidine gluconate (CHG), have also been reported to cause extensive burns in neonates (Fig. 8.9).35–37 Tissue damage can be prevented if the alcohol in the preparation is allowed to evaporate before draping for invasive procedures and carefully removed afterwards. Because of the reported incidence of CHG-related skin breakdown, use should be limited or avoided for VLBW infants.
Thermal injury
Scald injury and contact burns must be considered in the differential diagnosis of bullous lesions of unknown etiology. Inadvertent immersion injury was described in one such instance where the temperature of the hospital water supply was raised for purposes of infection control.38 Contact with a disposable warmer causing cicatricial alopecia and a cranial defect requiring bone grafts was reported in another neonate.39 Reports of deep burn injuries with relatively low-temperature (42°C) warming bottles have also been reported in the neonatal period.40,41
Burns related to attempts to warm hypothermic neonates with hot water-filled gloves or other items heated in a microwave have also been reported (Fig. 8.10).42 Scald burns become a much more common issue in older infants with non-accidental injuries, e.g. being forced to be immersed in very hot bath water.
Transillumination blisters
Thermal burns may occur as a complication of the use of transillumination devices for the detection of hydrocephalus, subdural effusions, cystic hygroma, pneumothorax, pneumomediastinum, or for localization of arteries and veins for blood sampling. Typical lesions are small (<5 mm), round, discrete blisters with a necrotic base that develop at sites of transillumination (Fig. 8.11).43 It is thought that specific wavelengths of the high-intensity fiberoptic light are converted to heat energy in the skin, causing thermal damage. Infrared and ultraviolet filters within the light source, usually a quartz halogen lamp, eliminate wavelengths of <570 nm, reducing the risk of thermal injury. A defect in the transilluminator unit, missing filters,44 prolonged contact with the skin or failure of the filter to function properly have accounted for the occurrence of these blisters in neonates.
Subcutaneous fat necrosis associated with therapeutic hypothermia
Therapeutic hypothermia has become the standard of care for treatment of hypoxic ischemic encephalopathy and has been shown to decrease mortality and reduce the incidence of long-term neurodevelopmental disability at 18–24 months’ follow-up.45 As a result, more tertiary neonatal units are utilizing this treatment modality and subcutaneous fat necrosis (SCFN) has been noted in some infants undergoing whole body cooling.45,46 SCFN can also be seen with perinatal hypoxia without therapeutic cooling,47 so infants cooled have an additional risk factor for this condition. SCFN is discussed in greater detail in Chapter 27.
Physical findings include firm nodules and plaques varying in color from flesh colored to erythematous, blue or purple.45 For the infant on cooling therapy, the areas most affected are those in contact with the cooling blanket, including the back, shoulders, upper arms, thighs, and buttocks (Fig. 8.12).46
Hypercalcemia occasionally complicates the course in these infants.48 Rarely, there is accompanying soft tissue calcification identifiable by biopsy or radiography.49 The presence of soft tissue calcification does not seem to portend a more ominous prognosis and eventually resolves. Preventative care involves frequent assessment of the skin, positional changes and the use of pressure-relieving mattresses and pillows.
Mechanical injury
Dermal stripping
Application and removal of adhesives and dressings can lead to inadvertent removal of the stratum corneum, pain, inflammation, edema, disrupted barrier function and increased transepidermal water loss (TEWL).50,51 For the preterm infant, the bond between adhesives and epidermis may be stronger than the bond between epidermis and dermis, leading to extensive tissue loss with adhesive removal (Figs 8.13, 8.14).51
Pressure ulcers
Pressure ulcers are defined as a localized injury to the skin and/or underlying tissue, usually over a bony prominence, due to pressure or pressure in combination with shear and/or friction (Fig. 8.15).52 The classification for pressure ulcers can be found on the National Pressure Ulcer Advisory Panel’s (NPUAP) website.53 The incidence of pressure ulcers has been reported to be as high as 23% in the neonatal intensive care unit (NICU) and 27% in the pediatric intensive care unit (PICU).54 A more recent multisite study of nine PICUs, including 5346 patients, showed the aggregate incidence of pressure ulcers to be 10.2%. The study found risk factors for development of pressure ulcers to include: age <2 years; PICU stay of >4 days; and treatment including the use of BiPAP, CPAP, conventional mechanical ventilation, high frequency oscillatory ventilation (HFOV) and extracorporeal membrane oxygenation (ECMO) (Fig. 8.15A,B).55 Neonates and infants with limited mobility, neuromuscular immaturity, hemodynamic instability, decreased sensory perception, and dependence on their caregivers for positional changes, are at increased risk of skin breakdown (Fig. 8.15C). Because of their disproportionately large head relative to body size, the most common site for pressure ulcer development in the infant is the occiput (Fig. 8.15D).54,56 Scarring alopecia of the occipital scalp has been documented as a consequence of ischemia and compromised oxygenation, or as a complication of extracorporeal membrane oxygenation (ECMO) therapy in neonates.57 During a 6-month period, five infants in a neonatal ICU were observed to develop erythema and edema that progressed to crusted ulcerations (Fig. 8.15E) and resulted in a patch of scarring alopecia (Fig. 8.15F). The ulcers were believed to be the result of prolonged pressure in a setting of hypoperfusion, acidosis, and hypoxemia. The institution of a protocol requiring frequent repositioning of the head and use of a temperature-stable gel pad as preventive measures, eliminated this problem.
For the VLBW infant, the combination of lengthy hospitalization, immature skin and dependence on medical devices increases the risk for pressure-related injury (Fig. 8.15G,H). Use of nasal continuous positive airway pressure (NCPAP) has been correlated with development of pressure ulcers in the preterm infant (Fig. 8.15I). The greatest risk factors include gestational age <32 weeks; birthweight <1500 g; >5 days on NCPAP, and >14-day stay in the NICU.58 Case reports of forehead pressure necrosis from the CPAP apparatus with resultant scarring and alopecia have also been published (Fig. 8.15J).59
Use of a validated assessment tool such as the Braden Q Scale60
