Study guide
4.1 Early Postmortem Changes: Algor, Livor, and Rigor Mortis Kinetics
ABMDI Board Certification Fellow
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1 Chapter 1: Performance Section Mastery & Medicolegal Scene Documentation
1.1 Board Exam Architecture, Scoring, and the Performance Section 1.2 Professional Scene Narrative Drafting & Medical Terminology 1.3 Strategic Investigative Interviewing for Witnesses and Suspects 1.4 Physical, Biological, and Trace Evidence Identification & Prioritization 1.5 The Advanced Skills List: The Official 46-Task Blueprint
2 Chapter 2: Legal Framework, Jurisdiction, and Interagency Coordination
2.1 Medicolegal Systems in the United States & Statutory Authority 2.2 Jurisdictional Boundaries & Federal Interagency Liaison 2.3 Accreditation Standards (NAME, ANAB/ISO 17020, IAC4MR) & Office Operations 2.4 Health Information Privacy (HIPAA § 164.512(g)), Public Records, and Subpoenas 2.5 Reviewing a Death Certification: Cause, Manner, and the Certifier’s Role 2.6 Unique Case Problems and Soliciting Legal Opinions
3 Chapter 3: Scene Leadership, Command Structure, and Processing Protocols
3.1 Incident Command System (ICS) Integration & Scene Leadership 3.2 OSAC ASB Standard 037 Protocols & Scene Security Management 3.3 Forensic Photography, Oblique Lighting, 3D Laser Scanning & Mapping 3.4 Search Methodologies, PPE Tiers & Cross-Contamination Controls 3.5 Masqueraded and Staged Death Scenes 3.6 Media-Sensitive Deaths and Public Information Management
4 Chapter 4: Postmortem Changes, Taphonomy, and PMI Estimation
4.1 Early Postmortem Changes: Algor, Livor, and Rigor Mortis Kinetics 4.2 Decomposition Chemistry, Autolysis, Putrefaction & Specialized Taphonomy 4.3 Forensic Entomology, Insect Succession & ADH/ADD Calculations 4.4 Forensic Anthropology, Skeletal Recovery & Biological Profiling
5 Chapter 5: Mechanical Trauma: Blunt, Sharp, and Ballistic Injuries
5.1 Blunt Force Trauma: Abrasions, Contusions, Lacerations & Skeletal Fractures 5.2 Sharp Force Trauma: Incised, Stab, Chop Wounds & Defensive Patterns 5.3 Firearm Injuries, Range of Fire Determinations & Terminal Ballistics 5.4 Motor Vehicle, Pedestrian Strike & Transportation Incident Dynamics 5.5 Explosion and Blast Injury Deaths
6 Chapter 6: Asphyxial, Environmental, and Thermal Deaths
6.1 Asphyxial Deaths: Hanging, Ligature/Manual Strangulation & Positional Asphyxia 6.2 Drowning Mechanisms, Submersion Injuries & Aquatic Recovery 6.3 Fire Deaths, Inhalation Injuries, COHb/Cyanide & Heat Alterations 6.4 Environmental Extremes: Hypothermia, Hyperthermia, High/Low Voltage Electrical & Lightning Deaths 6.5 Weather-Related and Natural-Disaster Deaths
7 Chapter 7: Forensic Toxicology, Specimen Protocols, and Natural Deaths
7.1 Postmortem Specimen Collection Sites, Anticoagulants & Chain of Custody 7.2 Postmortem Redistribution (PMR), Vd & Toxicological Pharmacokinetics 7.3 Opioids, Fentanyl Analogs, Novel Psychoactive Substances & Screening Limits 7.4 Sudden Unexpected Natural Deaths: Cardiovascular, Cerebrovascular & Pulmonary 7.5 Deaths from Therapeutic Complications and Medical Misadventure 7.6 Deaths from Infectious Causes and Public Health Reporting
8 Chapter 8: Pediatric, Infant, and Vulnerable Population Investigations
8.1 Sudden Unexpected Infant Death (SUID/SUDI) Protocols & CDC Doll Re-enactment 8.2 Abusive Head Trauma (AHT), Non-Accidental Skeletal Injuries & Scalds 8.3 Elder Abuse/Neglect, In-Custody Deaths & Excited Delirium/Restraint Analysis 8.4 Deaths in Extended Care Facilities and Group Homes 8.5 Deaths Caused by Animals and Postmortem Animal Activity
9 Chapter 9: Mass Fatality Management, Ethics, and Expert Testimony
9.1 Mass Fatality Incidents, DMORT Operations & DVI Scientific Identifications 9.2 Family Assistance Centers, Antemortem Records & OSAC ASB Std 038 Next-of-Kin Notifications 9.3 ABMDI Code of Ethics, Supervisory QA Audits & Investigator Resiliency 9.4 Medicolegal Testimony & Evidence Admissibility 9.5 Leadership: Mentoring, Correcting Deficiencies, and Personal Performance Standards 9.6 Serology, Bloodstain Pattern, and Tool Mark Evidence Collection
4.1 Early Postmortem Changes: Algor, Livor, and Rigor Mortis Kinetics
Key Takeaways Explain This Topic AI
Algor mortis cooling kinetics follow a sigmoid curve rather than a simple linear slope, characterized by an initial postmortem temperature plateau lasting 1 to 3 hours before entering an exponential cooling phase modeled by the Henssge nomogram.
Livor mortis transitions from blanching (unfixed) to non-blanching (fixed) between 8 and 12 hours postmortem; dual livor patterns provide incontrovertible physical evidence that a decedent's body position was altered after partial hypostatic fixation.
Atypical coloration of livor mortis provides critical diagnostic indicators: cherry-red or bright pink indicates carbon monoxide intoxication, cyanide poisoning, or hypothermic exposure; chocolate-brown indicates methemoglobinemia; and deep cyanotic purple indicates profound hypoxic terminal states.
Rigor mortis develops biochemically due to postmortem adenosine triphosphate (ATP) depletion preventing actin-myosin cross-bridge dissociation, following Nysten's law in its apparent clinical progression from smaller cranial muscles to larger distal limb groups.
Cadaveric spasm represents an instantaneous postmortem muscular contracture occurring at the exact moment of death without a preceding period of primary muscular flaccidity, typically associated with intense physical stress, violent struggle, or severe cerebral trauma.
Last updated: September 2026
Biophysical Kinetics of Algor Mortis and Mathematical Modeling
Algor mortis describes the postmortem reduction of core body temperature following the irreversible cessation of homeostatic metabolic thermogenesis. In living humans, core body temperature is tightly maintained by hypothalamic autonomic regulation within a narrow physiologic window (typically 36.5 ∘ C 36.5^\circ\text{C} 36. 5 ∘ C to 37.5 ∘ C 37.5^\circ\text{C} 37. 5 ∘ C or 97.7 ∘ F 97.7^\circ\text{F} 97. 7 ∘ F to 99.5 ∘ F 99.5^\circ\text{F} 99. 5 ∘ F ). Upon somatic death, active heat production ceases while passive thermal dissipation continues through four fundamental biophysical mechanisms: conduction , convection , radiation , and evaporation .
The Sigmoidal Cooling Curve vs. Newton's Law of Cooling
Early forensic literature frequently cited a crude rule of thumb stating that a corpse cools at an arbitrary linear rate of approximately 1.5 ∘ F 1.5^\circ\text{F} 1. 5 ∘ F ( 0.8 ∘ C 0.8^\circ\text{C} 0. 8 ∘ C ) per hour during the first 12 hours, and 1.0 ∘ F 1.0^\circ\text{F} 1. 0 ∘ F ( 0.5 ∘ C 0.5^\circ\text{C} 0. 5 ∘ C ) per hour thereafter. For the Board-Certified Fellow (F-ABMDI), relying on such linear simplifications is scientifically untenable and legally vulnerable in court. Human cadaveric cooling does not follow a linear slope; rather, it follows a sigmoidal (S-shaped) cooling curve . Core Temp (^C)
- 37 |-----\_ (Initial Temperature Plateau: 1 to 3 hours)
- | \
- | \ (Steep, Quasi-Linear Convective/Conductive Cooling)
- | \
- | \_
- 20 | \_________________ (Asymptotic Approach to Ambient Temp)
- +----------------------------------> Time Postmortem (Hours)
The sigmoidal curve comprises three discrete kinematic phases:
The Postmortem Temperature Plateau: For the initial 1 to 3 hours (and up to 5 hours in heavily insulated or obese decedents), central core temperature remains virtually unchanged. Heat continues to transfer from inner visceral organs (liver, mesenteric core) to the outer somatic shell, while peripheral tissues cool first. Until a thermal gradient between the deep visceral core and the skin surface is established, internal core cooling is delayed.
The Intermediate Exponential Phase: Once the thermal gradient is fully established, heat loss accelerates rapidly into a quasi-linear decline, governed largely by Newton's law of cooling, which dictates that the rate of heat loss is directly proportional to the temperature differential between the body and its surrounding ambient medium.
The Asymptotic Terminal Phase: As the core body temperature approaches the ambient environmental temperature, heat transfer slows exponentially, forming a long asymptotic tail that can persist for many hours until thermal equilibrium is achieved.
The Henssge Nomogram for PMI Estimation
To date, the most scientifically validated, single-measurement method for calculating the early postmortem interval (PMI) based on algor mortis is the Henssge Nomogram (developed by Claus Henssge in 1979 and refined through multiple international trials). Henssge's double-exponential equation accounts for body mass, ambient temperature, and site-specific rectal cooling curves, providing a mean PMI estimate with a 95% confidence limit ( 2 σ 2\sigma 2 σ ), typically within ± 2.8 \pm 2.8 ± 2.8 to ± 4.5 \pm 4.5 ± 4.5 hours under controlled settings.
Operational Parameters Required for Nomogram Execution
To execute a valid Henssge nomogram calculation, the investigator must collect four empirical parameters at the scene:
Deep Rectal Temperature ( T R T_R T R ): Measured using a dedicated, calibrated digital thermistor probe inserted at least 8 to 10 cm into the rectum, leaving the probe undisturbed for a minimum of 2 to 3 minutes until numeric equilibrium is achieved. Alternatively, deep hepatic temperature ( T H T_H T H ) can be recorded via a small subcostal stab incision directly into the right hepatic lobe if rectal pathology, sodomy trauma, or anal sexual assault evidence must be preserved pristine.
Ambient Environmental Temperature ( T A T_A T A ): Recorded at the exact level of the remains (not at room ceiling level or from an outdoor weather app). If the body is on a concrete basement floor, ambient temperature must be recorded directly at the floor-body interface and in the micro-ambient air 10 cm above the torso.
Body Mass ( W W W ): The total weight of the decedent in kilograms. Accurate weight is vital because thermal inertia is a direct function of body mass (large mass retains thermal energy substantially longer than pediatric or cachectic mass).
Correction Factor ( c c c -factor): An empirical multiplier adjusting for clothing, coverings, air currents, and surrounding media:
- Scene Condition / Substrate Henssge Correction Factor ( c c c )
- Naked body, still air 1.0 (Standard baseline)
- Lightly clothed (underwear, shirt), still air 1.1 - 1.2
- Moderately clothed (shirt, trousers, socks), still air 1.2 - 1.3
- Heavily clothed (winter coat, sweater, trousers) 1.3 - 1.5
- Heavy bedding / thick down quilt 1.8 - 2.4
- Wet clothing, still air 0.9 - 1.0 (Latent heat of evaporation accelerates cooling)
- Flowing water (river, stream) 0.5 (Rapid convective heat dissipation)
- Stagnant water (pool, bathtub) 0.7 - 0.8
Caution
Board Exam Trap: Antemortem Thermal Derangements The Henssge nomogram assumes a normal physiological antemortem core temperature of 37.2 ∘ C 37.2^\circ\text{C} 37. 2 ∘ C ( 99.0 ∘ F 99.0^\circ\text{F} 99. 0 ∘ F ). If the decedent experienced antemortem hyperthermia (e.g., lethal psychostimulant toxicity from cocaine or methamphetamine, exertional heat stroke, status epilepticus, or septic shock) where core temperature reached 41.0 ∘ C 41.0^\circ\text{C} 41. 0 ∘ C ( 105.8 ∘ F 105.8^\circ\text{F} 105. 8 ∘ F ), the investigator using standard nomogram charts will significantly underestimate the postmortem interval (calculating that the body died much later than it actually did). Conversely, antemortem hypothermia causes a dramatic overestimation of PMI. The investigator must interrogate the scene context for signs of agitated delirium, heavy sweating prior to collapse, heating pad use, or open space heaters.
Livor Mortis (Postmortem Hypostasis): Kinetics, Fixation, and Pathognomonic Patterns
Livor mortis (also termed postmortem hypostasis , suggillations , or vibices ) is the gravitational pooling and settling of blood within the capillaries, post-capillary venules, and small veins of the dependent regions of the body following the cessation of cardiovascular pressure.
Kinetics of Hypostasis
Early Onset (0.5 to 2 Hours): Hypostasis begins immediately upon cardiac arrest. Red blood cells settle through passive gravitational sedimentation. Within 30 minutes to 2 hours, faint, mottled, pink-to-purple patches appear in dependent skin areas.
Confluence and Extension (2 to 6 Hours): The individual mottled patches coalesce into continuous, uniform sheets of deep violaceous discoloration across all non-compressed dependent anatomy.
Blanching Phase (0 to 8 Hours): If firm, perpendicular digital pressure is applied to an area of livor mortis, or if a clear glass or acrylic slide is pressed against the skin (the diascopy test ), the pooled intravascular erythrocytes are mechanically displaced from the local capillary beds. The pressed area turns stark white ( blanches ) and slowly recolors upon pressure release. Blanching confirms that livor mortis is unfixed .
Fixity (8 to 12+ Hours): Over time, two microscopic processes occur: vascular permeability increases as endothelial tight junctions break down during autolysis, allowing hemolyzed erythrocytes to escape into perivascular interstitium, while concurrent hemoconcentration and intravascular coagulation trap packed erythrocytes inside degraded microvessels. Once this occurs, digital pressure fails to displace the pigment. The discoloration remains permanent and non-blanching . In temperate indoor environments ( 20 ∘ C 20^\circ\text{C} 2 0 ∘ C / 68 ∘ F 68^\circ\text{F} 6 8 ∘ F ), fixity typically becomes complete between 8 and 12 hours postmortem, though severe refrigeration can prolong blanchability for up to 24 to 36 hours. +-------------------------------------------------------------------------+
- | LIVOR MORTIS TIMELINE & KINETICS |
- +-------------------------------------------------------------------------+
- 0h ------------------ 2h ------------------ 8h ------------ 12h+ -------->
- Somatic Death Early Onset Confluent Livor Complete Fixity
- Cardiac Arrest Patchy Mottling Blanches Easily Non-Blanching
- (Intravascular) (Movable) (Tissue Stained)
- Dual Livor (Shifting of Hypostasis) and Scene Reconstruction
Dual livor represents one of the most powerful diagnostic tools available to the medicolegal death investigator to prove postmortem body alteration or staging:
If an individual dies in a prone position, livor initially accumulates on the anterior thoracic cage, abdomen, and anterior thighs. If the body is discovered lying supine , but exhibits non-blanching anterior livor along with secondary posterior blanching livor, the investigator has indisputable physical evidence that the remains were moved after death .
Specifically, this pattern demonstrates that the decedent remained prone for at least 4 to 8 hours (long enough to initiate substantial perivascular staining and microvascular packing), and was subsequently flipped into a supine position before complete fixation had locked all available blood in place.
Contact Pallor
Contact pallor occurs where external surfaces, firm structures, or constrictive clothing exert mechanical pressure exceeding hydrostatic capillary pressure, preventing blood from pooling in those specific zones. Hallmark examples include:
Anatomical pressure points: In a supine body, the scapulae, buttocks, posterior calves, and heels remain pale because they bear the body's gravitational weight against the substrate.
Clothing artifacts: Tight brassiere bands, belts, waistbands, sock elastic, and necklace chains produce distinct pale geographic bands bordering dark livor. These patterns must be photographed in situ to prove they are mechanical contact pallor rather than blunt force contusions or ligature strangulation marks.
Diagnostic Livor Coloration and Toxicological Correlation
Standard livor mortis presents as a dull reddish-purple or violaceous hue, reflecting deoxygenated hemoglobin. Deviation from this baseline provides immediate diagnostic insight:
Coloration Pathophysiological Mechanism Diagnostic Etiology
Cherry-Red / Bright Pink Formation of carboxyhemoglobin ( C O H b > 30 % COHb > 30\% CO H b > 30% ); bright red complex blocks oxygen delivery Carbon monoxide ( C O CO CO ) poisoning (fires, faulty heaters, motor vehicle exhaust)
Bright Pink / Brick Red Severe histotoxic hypoxia; cyanide binds cytochrome c c c oxidase, halting cellular oxygen extraction, leaving venous blood fully saturated with oxyhemoglobin Acute cyanide toxicity (potassium/sodium cyanide ingestion or industrial inhalation)
Bright Pink / Peachy Red Cold-induced shift of oxygen-hemoglobin dissociation curve to the left (Bohr effect in reverse); dermal capillaries re-oxygenate via atmospheric diffusion across thin, hypothermic skin Prolonged environmental hypothermia, cold storage, refrigeration, or ice immersion
Chocolate-Brown / Slate Gray Oxidation of ferrous iron ( F e 2 + Fe^{2+} F e 2 + ) to ferric iron ( F e 3 + Fe^{3+} F e 3 + ), forming methemoglobin ( M e t H b MetHb M e t H b ), which cannot bind oxygen Methemoglobinemia (ingestion of nitrites/nitrates, aniline dyes, dapsone, chlorates, toxic well water)
Dark Purple / Black-Blue Extreme systemic hypoxemia with maximal capillary venous congestion and elevated reduced hemoglobin Mechanical asphyxiation (hanging, positional asphyxia, crush asphyxia), severe COPD, congestive heart failure
Bronze / Green-Brown Massive postmortem hemolysis coupled with bacterially generated sulfhemoglobin Clostridium perfringens septicemia (septic abortion, gas gangrene, enterotoxemia)
Tip
Differentiating Cherry-Red Livor Causes at the Scene While carbon monoxide, cyanide, and cold exposure can all present with bright pinkish-red livor, scene investigation provides rapid deconfliction: CO is confirmed by an on-scene CO-oximeter or toxicological analysis of femoral blood; cyanide frequently presents with a faint "bitter almond" scent (though genetic anosmia prevents approximately 40% of the population from smelling it) and gastric erosion on autopsy; cold exposure is verified by scene ambient temperature, paradoxical undressing, terminal burrowing ( hide-and-die syndrome), and purple-red erythematous patches over the extensor surfaces of major joints (Wischnewsky spots are found internally on gastric mucosa at autopsy).
Rigor Mortis: Molecular Pathophysiology, Kinetics, and Muscular Pathology
Rigor mortis is the postmortem stiffening of skeletal, cardiac, and smooth musculature resulting from the loss of cellular metabolic energy. Unlike living muscular contraction, which is a dynamic, energy-consuming physiological event, rigor mortis is a state of physicochemical contracture driven by the complete exhaustion of adenosine triphosphate (ATP).
Molecular Mechanism of the Rigor Mortis Lock
In living muscle, muscle contraction occurs when calcium ions ( C a 2 + Ca^{2+} C a 2 + ) release from the sarcoplasmic reticulum, binding troponin and exposing binding sites on the actin filament. The myosin head binds actin, performs its "power stroke," and then requires the binding of a new ATP molecule to detach the myosin head from the actin filament, permitting muscle relaxation.
Following somatic death, cellular oxidative phosphorylation ceases instantly. Muscle cells transiently regenerate ATP through anaerobic glycolysis and the creatine phosphokinase pathway (creatine phosphate breakdown). Once glycogen stores and creatine phosphate are depleted, cytoplasmic ATP concentration falls below a critical threshold (approximately 15% of normal physiological levels).
In the absence of ATP, calcium ions diffuse unchecked from the degenerating sarcoplasmic reticulum into the sarcomere, initiating cross-linking between actin and myosin filaments. Without free ATP to bind the myosin head, the actin-myosin bridges remain permanently locked in place—a state known as the rigor mortis complex or rigor lock . Living Muscle: Actin + Myosin-ATP ---> Muscle Relaxes (Myosin detaches)
- Postmortem State: ATP Depleted ---> Actin-Myosin permanently locked ---> RIGOR MORTIS
- Nysten's Law and Progression Kinetics
Historically, the French pediatrician Pierre-Aimé Nysten (1811) formulated Nysten's Law , which states that rigor mortis appears sequentially in the following order: the muscles of the face and jaw (temporalis, masseter), followed by the neck, upper extremities, trunk, and finally the lower extremities.
Modern biomechanical research clarifies that ATP depletion and actin-myosin locking occur simultaneously in all muscle beds throughout the body . However, because smaller joints (temporomandibular joint, interphalangeal joints of the hand) contain substantially smaller muscle masses, their resistance to passive manipulation becomes clinically detectable to the investigator much sooner than in massive joint groups such as the hips, knees, or shoulders. Thus, Nysten's law remains clinically valid as a rule of physical examination.
Rigor Mortis Timeline (Temperate Environment: 20 ∘ C 20^\circ\text{C} 2 0 ∘ C / 68 ∘ F 68^\circ\text{F} 6 8 ∘ F )
0 to 2 Hours: Primary flaccidity. Muscles are relaxed; joints are fully movable.
2 to 4 Hours: Onset of detectable rigor in the masseters, jaw, and neck.
4 to 8 Hours: Extension of rigidity through the shoulders, elbows, wrists, and trunk.
8 to 12 Hours: Full development (peak rigidity); body is stiff ("board-like"); joints cannot be bent without significant mechanical force.
12 to 24 Hours: Rigor remains fully maintained and rigid.
24 to 36+ Hours: Progressive resolution of rigor (secondary flaccidity), beginning in the face and moving downward to the lower extremities, returning the body to a flaccid state.
The Resolution of Rigor Mortis
The resolution of rigor mortis is not caused by ATP regeneration. Rather, it is driven by endogenous autolysis and proteolysis . Hydrolytic lysosomal enzymes, specifically calpains and cathepsins , systematically digest and dismantle the protein infrastructure of the sarcomere—specifically cleaving titin, nebulin, and the Z-disc anchors. Once the structural protein scaffolds undergo enzymatic liquefaction, the actin-myosin lock collapses, resulting in permanent secondary muscular flaccidity.
Breaking Rigor Mortis: The Medicolegal Rule
When an investigator forcibly manipulates a joint to evaluate range of motion, the mechanical action physically tears the microscopic actin-myosin bridges and surrounding myofilaments:
If rigor mortis is incomplete (still in its developing phase, e.g., 3 hours postmortem), breaking the rigor will allow partial re-formation of stiffness, because unexpended residual glycogen and ATP continue to decline, forming new cross-bridges in the newly positioned limb.
If rigor mortis is fully developed (peak rigidity, 8 to 12 hours), forcibly breaking the rigor destroys the cross-bridges permanently. Rigor will never re-form in that muscle group. Documenting whether rigor re-formed after transport manipulation helps establish whether death occurred within the early onset window or at peak fixity.
Cadaveric Spasm (Instantaneous Rigor)
Cadaveric spasm (cataleptic rigidity) is a rare, extreme manifestation of postmortem stiffening that occurs instantaneously at the moment of death , bypassing primary flaccidity entirely. It typically involves isolated groups of voluntary muscles (most frequently the hands and forearms).
Etiology: Cadaveric spasm requires severe, violent physical exertion, intense emotional stress, or catastrophic neurological damage immediately preceding the terminal event. Under these conditions, localized intracellular glycogen and ATP pools are completely exhausted in vivo at the instant of death, precipitating immediate, unyielding actin-myosin binding.
Medicolegal Significance: Cadaveric spasm cannot be simulated or produced artificially postmortem. If a decedent's hand is locked in a powerful, vice-like grip around a suicide weapon (such as a handgun or knife), or has tightly clutched riverbed weeds and gravel in a drowning incident, this provides irrefutable evidence that the object was grasped while the individual was alive at the moment of death. An assailant cannot stage cadaveric spasm by placing a weapon into a decedent's hand after death, as the fingers would simply hang loose during primary flaccidity.
Differential Diagnosis: Livor Mortis vs. Antemortem Ecchymosis (Bruising)
One of the most critical courtroom challenges for an investigator is defending the distinction between dependent livor mortis and antemortem blunt force contusions (ecchymoses). This distinction is summarized in the diagnostic comparison below:
Diagnostic Feature Livor Mortis Antemortem Ecchymosis (Contusion)
Intravascular vs. Extravascular Intravascular (blood is retained within intact capillary/venular lumen) Extravascular (blood has ruptured out of torn vessels into the interstitial connective tissue)
Gross Incision & Water Wash Test Incising the skin reveals clean tissue; blood washes out readily under a stream of running water Incising reveals dark, clotted blood firmly adherent to subcutaneous fat and fascial planes; does not wash out
Distribution Confined strictly to dependent, non-compressed anatomical regions Located anywhere on the body, corresponding directly to points of physical impact or traction
Surface Texture & Elevation Flat, level with surrounding skin; no swelling or induration Often elevated, swollen, indurated, accompanied by abrasions or tissue edema
Microscopic Histology Intact vessel walls containing packed erythrocytes; no tissue inflammatory response Disrupted vessels, interstitial hemorrhage, fibrin deposition, and early neutrophilic or histiocytic infiltration