Attorney Reference Cards

How was strangulation applied? (one hand, two hands, forearm/chokehold, ligature, knee/foot) · Was pressure continuous or intermittent? · Were multiple methods used?

How long did it last? Vascular occlusion can cause brain injury within seconds — loss of consciousness occurs within approximately 10 seconds of bilateral carotid occlusion.

Was the survivor also smothered, struck in the head, or shaken during the attack?

Changes in vision (tunnel vision, graying out, spots) · Changes in hearing (ringing, muffled sounds) · Ability to breathe, speak, or scream · Dizziness or pressure in the head or face.

Did the survivor lose consciousness or have memory gaps? Note: 49% of patients with amnesia did not recall losing consciousness — LOC is an imperfect measure of anoxia.

Indicative of brain dysfunction and potentially lethal strangulation.

Petechiae (conjunctival, facial, behind ears, oral mucosa) · Contusions from fingers or thumbs · Fingernail scratches · Ligature marks · Neck swelling or tenderness · Subconjunctival hemorrhage.

Laryngeal fractures (hyoid bone, thyroid cartilage) · Soft tissue hematoma or edema · Carotid or vertebral artery dissection · Stroke or intracranial hemorrhage · Anoxic brain injury.

CT angiography for vascular injury · MRI most sensitive for subtle injury, though forensic interpretive value is currently limited.

Genital mucosal tissue heals within 24–72 hours. The interval between the event and examination is a key variable in interpreting findings.

Posterior fourchette, fossa navicularis, and hymenal margin are primary injury sites. Precise anatomical documentation is essential to accurate clinical interpretation.

SANE-certified examiners are trained in colposcopy and standardized evidence collection protocols. Examiner qualifications are relevant to the reliability of documented findings.

Bruising, bite marks, and defensive injuries are frequently documented. A thorough exam includes full-body assessment, not only the anogenital region.

Notches, clefts, and anatomical variations are frequently within normal range. Accurate interpretation requires comparison against established normative standards and peer review.

When substances are a factor, timing of toxicology collection is critical. Screens vary in what substances they detect — the specific panel used should be reviewed.

Consistency of history with injury pattern · Evidence of prior unexplained injuries · Age and developmental stage of the child.

Multiple fractures after minor trauma at early age, blue sclera, osteopenia, wormian bones, dentinogenesis imperfecta (brittle or translucent teeth), family history of bone disease or "easy" fractures. Kinky hair may also be present when seen alongside other signs and symptoms, but is not significant as an isolated finding.

25.5% rate of Silent Type IV OI mistaken for CAN; 13.1% for other OI types. Classic findings are not always present in all patients.

Evaluation requires comprehensive medical history, incident history, physical examination, and radiographic imaging by qualified medical experts.

The umbrella term for physical abuse, neglect, emotional abuse, and sexual abuse of a minor. In forensic contexts, often used specifically to refer to suspected physical abuse cases involving injury patterns.

A genetic connective tissue disorder causing abnormally fragile bones that fracture easily, sometimes with little or no apparent cause. Also called "brittle bone disease." Caused by defects in the gene that produces type I collagen. There are multiple types (I–IV and beyond), with varying severity.

A genetic disorder of tooth development associated with OI. Affects the dentin (the layer beneath tooth enamel), causing teeth to appear translucent, blue-gray, or amber-colored. Teeth are weaker than normal and prone to wear and breakage. Its presence can support an OI diagnosis.

Small, irregular extra bones that form within the sutures (joints) of the skull. Named after Danish anatomist Ole Worm. Their presence — particularly when more than 10 are found — is associated with OI and other connective tissue disorders. Identified on skull X-rays or CT imaging.

A bluish tint to the whites of the eyes, caused by abnormally thin scleral tissue that allows the underlying choroid layer to show through. A classic — though not universal — sign of OI. More pronounced in infants and may fade with age.

Lower-than-normal bone mineral density, making bones weaker and more prone to fracture. In OI, osteopenia results from defective collagen production. Identified on bone density scans (DEXA) or visible on standard X-rays as abnormally "light" bone appearance.

The process of distinguishing between two or more conditions that share similar signs or symptoms. In fracture cases, a proper differential diagnosis rules out medical causes (such as OI, rickets, or metabolic bone disease) before attributing injuries to abuse.

Legal limit 0.08% in most states.

THC levels do NOT correlate with impairment.

Rapid metabolism, short detection window.

Include prescription and illicit varieties.

Include methamphetamine and ADHD medications.

Therapeutic vs. toxic levels vary significantly.