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Burns and sudden death
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- 2. Definition Burns area result of the effects of thermal injury on the skin and other tissues Human skin can tolerate temperatures up to 42-440 C (107-1110 F) but above these, the higher the temperature the more severe the tissue destruction Below 450 C (1130 F), resulting changes are reversible but >450 C, protein damage exceeds the capacity of the cell to repair
- 3. Classification According toDepth First-degree Burns (mild): epidermis Pain, erythema & slight swelling, no blisters Tissue damage usually minimal, no scarring Pain resolves in 48-72 hours Superficial Second-degree Burns: entire epidermis & variable dermis Vesicles and blisters characteristic Extremely painful due to exposed nerve endings Heal in 7-14 days if without infection Midlevel to Deep Second-degree Burns: Few dermal appendages left There are some fluid & metabolic effects Full-thickness or Third-Degree: entire epidermis and dermis, no residual epidermis Painless, extensive fluid & metabolic deficits Heal only by wound contraction, if small, or if big, by skin grafting or coverage by a skin flap
- 4. Burn Photos Mild Burn 2nd degreeBurn 1 hr 2nd degree Burn 1 day 2nd degree Burn 2 days
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- 6. Classification According toExtent Mild: 10% Moderate: 10-30% Severe: > 30% • Hospitalization for > 10% of body surface area Anatomic structure Surface area Head 18% Anterior Torso 18% Posterior Torso 18% Each Leg 14% Each Arm 9% Perineum 1% Infant Rule of Nines (for quick assessment of total body surface area affected by burns)
- 7. Kinds of Burns Scald Burn: most frequent in home injuries; hot water, liquids and foods are most common causes; above 65o C, cell death Flame Burn: due to gasoline, kerosene, liquified petroleum gas (LPG) or burning houses Chemical Burn: common in industries and laboratories but may also occur at home; acid is more common than alkali Electrical Burn: worse than the other types; with entrance and exit wounds; may stop the heart and depress the respiratory center; may cause thrombosis and cataracts Radiation Burn: from X-ray, radioactive radiation and nuclear bomb explosions
- 8. Burn Photos Scald BurnsFlame Burns
- 9. Burn Photos Chemical (Acid)Burns Radiation (Flash) Burns
- 10. Burn Photos Electrical Burns EntranceWounds Electrical Burns Exit Wounds Entrance wound of electrical burns from an overheated tool Severe swelling peaks 24-72 hrs after Electrical burns mummified 1st 2 fingers later removed
- 11. Pathologic Features Zoneof coagulation (necrosis): Superficial area of coagulation necrosis and cell death on exposure to temperatures >450 (primary injury) Zone of stasis (vascular thrombosis): Local capillary circulation is sluggish, depending on the adequacy of the resuscitation, can either remain viable or proceed to cell death (secondary injury) Zone of hyperemia (increased capillary permeability)
- 16. Burn Pathophysiology: Edema Injured tissue Increased permeability of entire vascular tree loss of water, electrolytes and proteins from the vascular compartment severe hemoconcentration Protein leakage resultant hypoproteinemia, increased osmotic pressure in the interstitial space Decreased cell membrane potential cause inward shift of Na+ and H2O cellular swelling In the injured skin, effect maximal 30 min after the burn but capillary integrity not restored until 8-12 hours after, usually resolved by 3-5 days In non-injured tissues, only mild and transient leaks even for burns >40% BSA
- 17. Burn Pathophysiology: Cardiac Cardiac output decreases due to: 1) Decreased preload induced by fluid shifts 2) Increased systemic vascular resistance caused by both hypovolemia and systemic catecholamine release 3) A myocardial depressant factor has been described that impairs cardiac function Cardiac output normal within 12-18 hours, with successful resuscitation After 24 hours, it may increase up to 2 ½ times the normal and remain elevated until several months after the burn is closed
- 18. Burn Pathophysiology: Renal Renal blood flow and GFR decrease soon after due to hypovolemia, decreased cardiac output, and elevated systemic vascular oliguria and antidiuresis develops during 1st 12-24 hours Followed by a usually modest diuresis as the capillary leaks seal, plasma volume normalizes, and cardiac output increases after successful resuscitation and coinciding with onset of the postburn hypermetabolic state, and hyperdynamic circulation
- 19. Burn Pathophysiology: Immunologic Mechanical barrier to infection is impaired because of skin destruction Immunoglobulin levels decreased as part of general leak and leukocyte chemotaxis, phagocytosis, and cytotoxic activity impaired The reticuloendothelial system's depressed bacterial clearance is due to decreases in opsonic function These changes, together with a non-perfused, bacterially-colonized eschar overlying a wound full of proteinaceous fluid, put the patient in a significant risk for infection
- 20. First Aid Measuresin Burns 1. Extinguish flames by rolling in the ground, cover child with blanket, coat or carpet 2. After determining airway is patent, remove smoldering clothes and constricting accessories during edema phase in the 1st 24-72 hours after 3. Brush off remaining chemical if powdered or solid then wash or irrigate abundantly with water 4. Cover burn wounds with clean, dry sheet and apply cold (not iced) wet compresses to small injuries; significant burns (>15-20% BSA) decreases body temperature which contraindicates use of cold compress dressings 5. If burn caused by hot tar, mineral oil to remove it
- 21. Outpatient Management For1st and 2nd degree burns less than 10% BSA Blisters should be left intact and dressed with silver sulfadiazine cream Dressings should be changed daily washing with lukewarm water to remove any cream left
- 22. Recommendations for Hospitalization 1.Total burns >10% BSA or >2% full thickness, halved for <2 or >40 yr 2. Hands, face, feet or genitalia involved 3. Evidence or suspicion of inhalation injury 4. Associated injuries present 5. Suspicion that burn inflicted 6. Burn is infected 7. Burn circumferential 8. History of prior medical illness 9. Patient is comatose 10. Patient or family unable to cope with situation
- 23. Hospital Management 1. Generalassessment and cardiopulmonary stabilization 2. Resuscitation 3. Establishment of IV lines and blood studies 4. Wound care and infection control 5. Pain relief and psychological support 6. Nutritional support 7. Physical Therapy/Occupational Therapy
- 24. Airway compromise? Respiratory distress? Circulatorycompromise? Intubation, 100% O2 IV access, fluids Multiple trauma? Yes No Evaluate & treat injuries Burns >15% or complicated burns? Yes No Burn care, tetanus prophylaxis, analgesia IV access; fluid replacement Circumferential full thickness burns? Escharotomy Yes YesNo No
- 25. Initial Procedures Fluidinfusion must be started immediately NGT insertion to prevent gastric dilatation, vomiting and aspiration Urinary catheter to measure urine output Weight important and has to be taken daily Local treatment delayed till respiratory distress and shock controlled Hematocrit and bacterial cultures necessary
- 26. Fluid Resuscitation Formost, Parkland formula a suitable starting guide (4 ml Ringer’s Lactate/kg body weight/% BSA burned), ½ to be given over 1st 8 hr from time of onset while remaining over the next 16 hr During 2nd 24 hr, ½ of 1st day fluid requirement to be infused as D5LR Oral supplementation may start 48 hr after as homogenized milk or soy-based products given by bolus or constant infusion via NGT Albumin 5% may be used to maintain serum albumin levels at 2 g/dl Packed RBC recommended if hematocrit falls below 24% (Hgb <8 g/dl) Sodium supplementation may be needed if burns greater than 20% BSA
- 27. Inhalation Injury Threesyndromes: 1. Early CO poisoning, airway obstruction & pulmonary edema major concerns 2. ARDS usually at 24-48 hrs or much later 3. Pneumonia and pulmonary emboli as late complications (days to weeks) Assessment: 1. Observation (swelling or carbonaceous material in nasal passages 2. Laboratory determination of carboxyhemoglobin and ABGs Treatment: 1. Maintain patent airway by early ET intubation, adequate ventilation and oxygenation 2. Aggressive pulmonary toilet and chest physiotherapy
- 28. Infection Control Tetanusprophylaxis: 250-500 IU TIG or 3000 units equine ATS ANST IM; Toxoid also Antibiotic of choice is one that will include Pseudomonas in its spectrum; most frequent pathogens in burns are Staphylococcus aureus, Pseudomonas aeruginosa and the Klebsiella- Enterobacter species Topical therapy: 0.5% Silver nitrate dressing Mafenide acetate or Sulfacetamide acetate cream Silver sulfadiazine cream Povidone-iodine ointment Gentamicin cream or ointment
- 29. Pain Relief andAdjustment Important to provide adequate analgesia, anxiolytics and psychological support to: a) Reduce early metabolic stress b) Decrease potential for posttraumatic stress syndrome c) Allow future stabilization and rehabilitation Family support patient through grieving process and help accept long-term changes in appearance
- 30. Nutritional Support ShrinersBurn Institute at Galveston, Texas Guidelines for Caloric Intake Infants 1000 kcal/m2 BSA burned + 2100 kcal/m2 total BSA 2-15 years 1300 kcal/m2 BSA burned + 1800 kcal/m2 total BSA Adolescents 1500 kcal/m2 BSA burned + 1500 kcal/m2 total BSA
- 31. Complications of Burns Burn Shock Pulmonary complications due to inhalation injury Acute Renal Failure Infections and Sepsis Curling’s ulcer in large burns over 30% usually after 9th day Extensive and disabling scarring Psychological trauma Cancer called Marjolin’s ulcer, may take 21 years to develop
- 32. Sudden death Definition: Unexpectedly death within 24 hrs from onset of symptoms with or without known preexisting conditions. In forensic view most of cases occur within minutes or even seconds from onset of symptoms . There are no obvious criminal or accidental causes, and becomes of some concern to the forensic pathologist simply because of the difficulty or even impossibility to furnish a certifiable cause of death. The numerous causes of sudden natural death may conveniently be classified according to the different anatomical systems of the body.
- 33. Causes of suddendeath Cardiovascular System Respiratory System Gastrointestinal System Gynecological conditions Central Nervous System Other
- 34. Heart •The heart ofan adult Indian –Male 275-300 g –Female 225-250g •Thickness –Atrial wall 1-2 mm –Right ventricle 3-5 mm –Left ventricle 10-15 mm •Layers of the heart –Outer epicardium –Middle myocardium –Inner endocardium •Heart enclosed by visceral and parietal pericardium
- 35. Heart The LeftCoronary Artery: originating from the left aortic sinus, after a short course, bifurcates into: –Left anterior descending which runs in the anterior inter-ventricular groove, provides blood to anterior left ventricle, the adjacent anterior right ventricle and anterior two thirds of the inter- ventricular septum –Left circumflex branch, which runs in left atrio- ventricular groove, supplies the lateral wall of the left ventricle
- 36. Heart The RightCoronary Artery runs in the right atrio- ventricular groove. It usually nourishes the remainder of the right ventricle and the postero- septal region of the left ventricle, including the posterior third of the inter-ventricular septum.
- 37. The localization of atheromaor thrombus Left anterior descending (left anterior inter- venrticular) (45-64%) •Right main coronary (45-46%) •Left circumflex coronary (3-10%) •Left main coronary (0-10%)
- 38. Heart causes ofsudden death Ischemic heart disease :the most common cause. Coronory atherosclerosis . HTN Aortic valve disease. Cardiomyopathies. Death in old ages.
- 39. Bridging Frequent causeof sudden death Presence of coronary blood vessels deep in myocardium (normally : epicardium). Myocardial contraction compromises the coronary blood flow .
- 40. RESPIRATORY SYSTEM PulmonaryEmbolism massive haemorrhage in the air passages Pneumothorax asthma Chest infections :H.influanza: fulminating epiglottis in pediatric , Diptheria: laryngeal obstruction.
- 41. GIT causes Bleeding: esophageal verices PUD CA in stomach or esopheus. Mesenteric infraction . Strangulated hernia. Fulminating peritonitis.
- 42. GUT Mostly relatedto pregnancy Ectopic pregnancy . Induced abortions: hemorrhage, air embolus, tract perforation.
- 43. Epilepsy Epileptic sufferers maydie during a prolonged single seizure or more usually during a series of repeated seizures termed status epilepticus Death is due to asphyxia if the epileptic ceases to breathe or aspirates regurgitated vomit, or has an airway obstructed by the tongue.