Thermal Injuries & Diseases PDF

Thermal Diseases & Injuries Dr. Isam Elhassan Introduction Any medical practitioner should have the basic knowledge: to diagnose fatal and non fatal thermal injuries. Normal body temperature and variations. Regulation. Effect of air movement Heat conduction by: ❑ Condu...

Thermal Diseases & Injuries Dr. Isam Elhassan Introduction Any medical practitioner should have the basic knowledge: to diagnose fatal and non fatal thermal injuries. Normal body temperature and variations. Regulation. Effect of air movement Heat conduction by: ❑ Conduction ❑ Conviction ❑ Radiation Introduction Thermal injuries are any injury caused by a defect in body temperature control or from the application of external heat. It can be caused by direct burns, corrosive chemicals, electric current, radiation and cold weather or drugs. Effect of Hypothermia Core temp less than24 – 32o C. Recovery is rare if rectal temp. below 26o C. - Skin: Cyanosed pale extremities, nose, ears fingers and toes. Pink to brownish discoloration of large joints and extensor surfaces. Blistering of the skin. Face appear as myxedema Acute gastritis, pancreatitis, pulmonary edema and brain perivascular hemorrhage Effect of Hypothermia Low heart rate, low BP. Depressed reflexes. Lethargy, drowsy. Stupor, coma and death. Frost bite: Local tissue necrosis PM: Pink hypostasis. Congested organs. Types of heat diseases Types of heat diseases Hyperthermia☹ (sun or heat stroke) Sun, industries (huge baking oven) or poorly ventilated rooms with moist, drugs (malignant hyperthermia) Due to the effect of heat, and the heat leads to degeneration of the heat regulating center in the hypothalamus then the body fail to loose heat Effect: Heat cramp, exhaustion and stroke. Presentation: - Core body temp. 39o C or above with absence of sweating. - Hot dry skin with increase depth of respiration. - Rapid thready pulse with decreased BP. - watery diarrhea, increase thirst and chest pain. - Pin point pupils. Hyperthermia☹ (heat stroke) Pulmonary edema. Haemoptysis + haematamisis due to DIC. Convulsion, delirium and stupor. Fainting, coma with Respiratory & cardiac failure leading to Death. Medico-legal importance –No but compensation. Postmortem: Normal PM cooling not observed, rigor set in and pass off earlier. Classification of burns: Dupuytren’s classification (old) : 1st 2nd 3rd 4th 5th 6th Wilson’s classification (recent) : 1st 2nd 3rd  1st degree : vascular reaction , reddening of the skin – then it returns completely to normal. 2nd degree : detachment of epidermis from dermis , dead tissue , oedema and outpouring of fluid and vesication. 3rd degree : tissue undergo massive necrosis. Carbonization can occur. Second degree burn with blisters (vesication) Third degree burn  Rule of nine (Wallace classification) - 20% fluid loss is marked. - 30 – 50% Fatal. - Site of the body involved, head & neck, trunk, lower abd., upper & lower limbs & genitalia. - Age of the patient, old more than children & adults.  Types of burns 1. Dry burn 2. Wet burn (Scald) 3. Chemical burn (Corrosives) 4. Electrical burn (electrocution) 5. Lightening 6. Radiation Dry burn Due to dry heat: ❑ Flame ❑ Hot object  Wet burn (Scald) Due to steam or hot water, oil or any liquid at boiling point. Moist heat involving superficial layers of skin. C\F: erythema, vesication and necrosis of the dermis. Medicolegal importance: Usually accidental, e.g. cooking or bathing. Accident is common in children and elderly. Suicide and homicide is extremely rare. Could be due to child abuse Could be antemortem or postmortem.  Chemical burn A chemical burn is irritation and destruction of human tissue caused by exposure to a chemical, usually by direct contact with the chemical or its fumes. Most chemical burns are caused by either strong acids or strong bases. Acids damage and kill cells by coagulating cells while bases liquefy cells. Prolonged exposure can severely damage human tissues and, if the patient survives, it leads to scarring and disability.  Chemical burn All chemical burns should be considered potential medical emergencies. Most chemical burns occur on the face, eyes, hands, arms, and legs.  Chemical burn Tissue damage from chemical burns depends on several factors : o The PH of the chemical o concentration of the agent o The site of contact (eye, skin, mucous membrane) o Whether swallowed or inhaled o Whether or not skin is intact o The duration of exposure  Chemical burn In severe cases, a person may develop: o Hypotension o Shortness of breath o Muscle twitching or seizures o Cardiac arrest or irregular heartbeat Chemical burn Chemical burn  Chemical burn Sulfuric Acid Concentrated sulfuric acid is extremely corrosive and can cause serious burns. If sulfuric acid makes direct contact with the eyes, it can cause permanent blindness. If ingested, it may cause internal burns, irreversible organ damage, and possibly death. Chemical burn Suicide with sulfuric acid Chemical burn alkali; NaOH Electrical burn (electrocution) or shock  Electrical burn (electrocution) or shock Passage of substantial electrical current through the tissues, mostly accidental or suicidal. There are two types of currents: DC : less dangerous. AC : most dangerous. Alteration of current causes “hold on” effect due to spasm of muscles. Usually leads to ventricular fibrillation. Low voltage currents causes ventricular fibrillation while high voltage current causes electrical burns. Electrical burn (electrocution) or shock  Electrical burn (electrocution) or shock Post- mortem findings : ► Asphyxia ► Blue hypostasis ( post-mortem lividity) ► Current marks ► “Crocodile” skin in severe electrical burns. Electrical burn (electrocution) or shock  Electrical burn (electrocution) or shock ‘Crocodile’ skin Cause of death in electric injuries: ❑ Directly: ► Ventricular fibrillation ► Respiratory failure ( central and peripheral) ► Eclectic burns ( 3rd degree) ❑ Indirectly: traumas Medical tools & appliances Lightning  Lightning “Ferning (filigree) or Lichten berg figure in lightning Lightning  Complications: Direct complications of burns: Massive cell necrosis , K+ release, hyperkalemia leading to cardiac arrest and immediate death. Shock – neurogenic ( due to intense pain or fear). Asphyxia due to epiglottis edema esp. in neck burns. Direct damage to vital organs (eg heart, liver, brain).  Complications due to loss of skin function: Shock- hypovolemic polycythemia ( due to fluid accumulation in interstitium and evaporation through damaged skin). Infection and sepsis esp. by Pseudomonas aeruginosa. Others: Protein loss and negative nitrogen balance. Pulmonary fat embolism if burn extends subcutaneously. Gangrene secondary to massive necrosis.  Post- mortem findings: Pugilistic/ boxer attitude(due to flexor muscles contraction). Skull thermal fractures. Heat hematoma Splits (cuts) on flexor surfaces of large joints Acute tubular necrosis with heme casts. Soot in trachea and air passages. Post- mortem findings: Cherry –red hypostasis (post-mortem lividity) due to carboxy-hemoglobin. Acute ulcer in esophagus, stomach and duodenum (curling ulcers). Heat brain herniation. Pugilistic/ boxer stance Cherry- red hypostasis Acute stress ulcers Mid term exam Dec, 2023 (5) What is your diagnosis? The End