The document details various environmental injuries, including cold-related, heat-related, electrical injuries, and drowning, along with their clinical signs, management, and prevention strategies. It covers specific conditions such as frostbite, hypothermia, heat stroke, and interventions for electrical and drowning incidents, emphasizing urgent care and monitoring. Furthermore, it highlights the incidence of various injuries in different demographics and outlines approaches to treat bites and stings from animals.

1. Environmental Injuries Cold-related Injuries Heat-related Injuries Electrical Injuries Submersion/Drowning CO Poisoning Bites and Stings

2. Cold-related Injuries

3. Cold-Related Conditions: Tissue Injury Frostbite Tissue is cold and lacks sensation Skin appears pale or mottled blue Feels waxy and firm Blisters, maceration and secondary bacterial infection can occur Trench Foot / Immersion Foot Tissue in wet, cold environment Patient complains of numbness, pain and paresthesias Initially pale, sensitive and edematous Later findings are erythema, mottling or cyanosis

4. Frostbite & Trench Foot

5. Treatments Frostbite Warm in 40 °C water Tetanus prophylaxis Analgesia Remove clear blister but NOT hemorrhagic blisters Indian Journal of Medical Research, July 2002; 116:29-34 Pentoxifylline Aspirin Vitamin C Trench/Immersion Foot Rewarm Remove wet clothing Elevate Local skin care Topical antibiotics Cleansing of denuded areas Avoid wet environment! Improves in 4-6 weeks

6. Hypothermia Core body temperature < 35 °C Clinical signs Mild: shivering, confusion, lethargy, ↑HR ↑RR Moderate: Shivering stops < 32°C, disoriented, stupor, ↓HR ↓BP ↓RR, decr reflexes Severe ( < 28 °C): coma, dilated unreactive pupils, absent reflexes, muscle rigidity, ↓HR ↓BP ↓RR,asystole, ventricular fibrillation

7. Hypothermia Cardiac Issues Mild: tachycardia Moderate: AF, PAT, PVCs, T-wave changes Osborne waves , J waves, or camel-hump most prominent in inferior and lateral leads Severe: bradycardia, asystole, VF

8. Osborne J Wave

9. Hypothermia Management ABC’s, IV, O 2 Continuous cardiac and temp monitoring Remove all wet clothes Rewarming stages Warm blankets (Bair Hugger) Warm (45 °C) IV fluids and humidified O 2 (45 °C) Core rewarming techniques Nasogastric tube, peritoneal lavage, pleuromediastinal lavage, femoro-femoral cardiopulmonary bypass Endocrine issues: consider steroids and thyroxine

10. Hypothermia Key Concept: Afterdrop or Rewarming Shock During rewarming, the core temperature may drop! Theory Core is warmer than periphery As you warm periphery, blood vessels dilate More cold blood moves to core Prevention Surface and core rewarming should occur simultaneously

11. Heat-Related Conditions Internal Heat Emergencies Malignant hyperthermia Neuroleptic malignant syndrome Serotonin syndrome External Heat Emergencies Heat cramps Heat edema Heat syncope Heat exhaustion Heat stroke

12. Heat: A Few Facts #2 environmental killer after hypothermia USA 1936 - 1975, nearly 20,000 deaths in U.S. 1979 – 1997, nearly 7,000 deaths Great heat wave of 1980: 1,250 deaths Average year: 175 deaths in the U.S. India 1998 – heat wave killed 2600 in 10 weeks (official #) 2003 – heat wave (50 °C or 122°F) killed > 1300 Future expectations Global warming Aging of the population Increase frequency and intensity of heat waves predicted

13. Risk Factors Children up to four years of age >65 years of age Mental or Physical Disability Overweight Overexertion during work or exercise

15. Heat Cramps Brief, intermittent, muscle cramping Abdominal rectus or calf muscles Euthermic, mild dehydration No need to check labs (CK or U/A) IV Fluids rarely required

16. Heat Edema Swollen feet/ankles after prolonged sitting/standing Typically in (semi)tropical areas Vasodilation, hydrostatic pressure and orthostatic pooling lead to vascular leak No underlying cardiac, lymphatic, hepatic or venous disease Elevate, support hose, reassurance Diuretics – no proven benefit

17. Heat Syncope Diagnosis of exclusion in young, healthy patients without cardiac problems! Syncopal event in warm/humid weather following strenuous activity Pooling of blood in periphery from vasodilation due to heat Euthermic, normal exam Hydrate!

18. Heat Exhaustion Similar to a viral syndrome Fatigue and weakness Nausea and vomiting Headache and myalgias Dizziness Muscle cramps and myalgias Irritability

19. Heat Exhaustion Physical Findings Weakness Vomiting Orthostatic pulse and blood pressure changes Sweating* Piloerection Tachycardia Temperature is usually less than 41°C (106°F) Normal mental status!

20. Heat Exhaustion Treatment Check electrolytes Check CPK and dip urine Aggressive rehydration with intravenous normal saline Endpoint: normothermic and good urine output

22. Heat Stroke: Definition Catastrophic life-threatening medical emergency that occurs when homeostatic thermoregulatory mechanisms fail Neurologic dysfunction induced by overwhelming hyperthermia

23. Diagnosis of Heat Stroke Exposure to heat stress, endogenous or exogenous Signs of severe CNS dysfunction (coma, seizures, delirium) Core temperature usually above 40.5° C (105° F), but may be lower Dry, hot skin common, but sweating may persist Marked elevation of hepatic transaminases

24. Exertional Healthy Younger Exercise Athletes/military recruits Sporadic Classical Unable to escape extreme thermal conditions Slower onset Predisposing factors Older, chronic illness Sedentary Heat wave occurrence Two Categories of Heat Stroke

25. Two Categories of Heat Stroke Exertional Diaphoresis Hypoglycemia DIC Rhabdomyolysis Acute renal failure Marked lactic acidosis Hypocalcemia Elevated LFT’s Classical Anhydrosis Normoglycemia Mild coagulopathy Mild CPK elevation Oliguria Mild acidosis/resp alkalosis Normocalcemia Elevated LFT’s

26. Heat Stroke End organ damage Central Nervous System Cardiovascular Coagulopathy Respiratory Renal and Metabolic Liver

27. Heat Stroke CNS dysfunction Sudden onset in 80% of cases Bizarre behavior Hallucinations Delirium Altered mental status Coma Seizures (75% of patients) Muscle rigidity with tonic contractions, tremors, and dystonic movements Permanent damage is common

28. Heat Stroke Cardiovascular Sinus tachycardia as high as 150 bpm Hypodynamic or hyperdynamic circulatory state Hypotension is a late finding

29. Heat Stroke Coagulopathy: DIC Purpura Conjunctival hemorrhage Melena GI bleeding Hematuria Myocardial bleeding CNS hemorrhage

30. Heat Stroke Respiratory Tachypnea Respiratory alkalosis Respiratory decompensation Acute respiratory distress syndrome

31. Heat Stroke Renal Failure 25% of exertional and 5% of classic Splanchnic constriction Diminished renal blood flow Rhabdomyolisis Myoglobinuria Hyperuricemia and urinary acidification DIC Glomerular damage

32. Heat Stroke Electrolyte Disorders Respiratory alkalosis followed by severe metabolic acidosis Early hypokalemia (response to respiratory alkalosis) Later hyperkalemia (induced by rhabdomyolisis and renal failure) Hyponatremia Hypocalcemia

33. Heat Stroke Hepatic Damage Consistent finding Transaminase rise > 10,000 Jaundice within 24-36 hours Recovery usual but case reports of liver failure requiring transplantation

34. Differential Diagnosis Infectious Meningitis, encephalitis Malaria, Typhoid fever, Typhus Thyroid Storm Delerium Tremens Hypothalmic Hemorrhage Toxic Adrenergic: Cocaine, PCP Anticholinergic: Tricyclic OD, Jimson Weed Neuroleptic Malignant Syndrome Malignant Hyperthermia

35. Differential Diagnosis Start treating overheating first! Consider alternatives when temperature does not respond to cooling Shaking chills (rigors) Enlarged thyroid gland Mydriasis (anticholinergic poisoning)

36. Work-Up CT Scan Head Tox Screen LFTs Coagulation profile Electrolytes and renal function ABG Thyroid function tests

37. Management of Heat Stroke Cooling should be initiated immediately Prehospital if possible Priority over diagnostic studies Delays increase mortality! Remove clothing Monitor temperature continuously

38. Cooling Modalities Goal: reduce temperature below 39°C (102.2°F) Evaporative cooling Ice-water immersion Ice packs to axillae and groin Cooling blanket Gastric lavage Rectal lavage Peritoneal lavage (unproven efficacy in humans) Cardiopulmonary bypass

39. Evaporative cooling Body Cooling Unit Spray with atomized 15° C water from above and below Air warmed to 45° to 48° C is blown over the skin surface at 3 m/min or Combination of atomized tepid water at 40° C from a spray bottle and standing fans

40. Ice-water emersion Rapid lowering of the core temperature to 39°C (102.2°F) in 10 to 40 minutes Cold-water immersion Similar rates of cooling Less uncomfortable Problems Peripheral vasoconstriction shunting of blood away from the skin raised core body temperature Induced shivering Difficulty in resuscitating the patient

41. Other modalities Airway management and PPV Intravenous fluids slowly (watch out for elevating ICP) Mannitol Steroids not helpful Dantrolene: No proven benefit Antibiotics - if infectious etiology

42. A few don’ts Acetaminophen Aspirin Atropine/anticholinergics Alcohol sponge baths Don’t give up easily Reports of recovery in patients with T 115.7 ºF

43. Electrical Injuries Incidence 2/3 of high voltage electricity injuries occur in electrical, construction and industrial workers 30% of all injuries occur in children and adolescents Physics Current (amps) = Voltage / Resistance Voltage is all we generally know Nerves, blood and muscle are rich in electrolytes and have lowest tissue resistance Tissue conduction: nerve>blood>tissue & muscle>fat>bone AC current is more dangerous than DC current Exit wound of AC current larger!

44. Spectrum Sudden death Cardiac dysrhythmias – 25% Tissue injuries (external and internal) Unpredictable course of electricity thru body External signs limited and deceptively benign Neurologic dysfunction CNS: amnesia, AMS, irritability, depression, seizure, motor deficit, resp depression, coma (often transient) PNS: very common at point of contact Trauma Internal: vascular thrombosis, muscle damage (coag necrosis) External: tetanic muscular contractions and falls lead to shoulder dislocation, long bone fracture, and spinal compression fractures

45. Management of High-Tension Electrical Injury Evaluate as if multiple trauma patient ABCs Immobilize cervical spine IV fluids, O 2 , monitor 12-lead ECG Extensive resuscitative measures for cardiopulmonary arrest Limb dysfunction Consider compartment syndrome Ischemic limb Tetanus

46. Lightning Massive DC electrical shock: 2,000 to 2 billion volts 75-300 deaths and 1500 injuries per year (USA) 20% mortality – cardiac asystole followed by resp arrest “ Flash-over” phenomenon Current passes over outside of body because of very short duration Entrance and exit burns rare 50% with structural eye lesions Cataracts, retinal detachment Hyphema, iritis Unreactive, dilated pupil from autonomic instability (not brain damage!) 50% with ruptured TM (blast/thunder component) Paraplegia and amnesia are relatively common

47. Lichtenberg Figures Due to Lightning Strike

48. Few Rules Delayed labial artery bleeding! Exposure to > 600 Volts should be monitored overnight

49. Submersion/Drowning Injuries Drowning: death from suffocation due to submersion Wet drowning (85-90%): fluid is aspirated Dry drowning: fluid is not aspirated; laryngospam occurs Secondary drowning: ARDS/non-cardiogenic pulmonary edema 8,000 deaths/year in the U.S. Highest incidence in 10-19 age group 40% of victims are less than 4 years old Male:Female ratio = 5:1 600x more submersion injuries than deaths Key factors Alcohol and drug use Inability to swim Seizures

50. Near Drowning Injuries Hypoxia Diffusion abnormalities and decreased lung compliance Surfactant inactivated/diluted by aspirated water Intrapulmonary shunting Atelectasis Bronchospasm Obstruction of alveoli by water Acidosis Respiratory cause: hypoventilation Metabolic cause: hypoperfusion leads to lactate production Cardiovascular complications Cardiac arrest and hypotension >> VF Hypothermia Rare complications Renal failure due to hypoxia or rhabdomyolysis DIC

51. Neurologic Injury 15-25% of near-drowning victims Cerebral edema Hypoxia Acidosis Favorable outcome Immediate CPR Hypothermia Key Fact: Of patients that present in coma with fixed and dilated pupils, 10-20% have complete recovery!!!

52. Submersion Injuries Evaluation History: as detailed as possible Focused physical Exam Vitals: rectal temperature! Cardiopulmonary and neuro status Evidence of trauma ECG Labs, including ABG Head CT

53. Submersion Injuries Management IV, O2, monitor, remove wet clothing CPR Airway Clear debris Intubate and place on PEEP Persistent hypoxia may require suctioning and bronchoscopy Albuterol for bronchospasm Consider sodium bicarbonate empirically Gastric decompression Not proven to be helpful Steroids Antibiotics Induced hypothermia

54. Carbon Monoxide Colorless, odorless gas Produced by combustion of any carbon-containing material Sources Faulty heating Closed-space fire Defective automobile exhaust Combustion Statistics:1979-1988 (10 year period) 56,133 deaths due to CO poisoning 25, 889 were suicides 15,523 associated with severe burns or house fires 11,547 were unintentional

55. CO Poisoning Mechanism Combines with hemoglobin with affinity 250x greater than oxygen Shifts oxygen-Hgb dissociation curve Results: hypoxia, ischemia, cellular asphyxia Half-life in room air = 4-5 hours

56. CO Poisoning CO Level Signs & Symptoms 0-10 none 10-20 headache, dyspnea on exertion 20-30 headache, dyspnea, nausea, dizziness 30-40 severe HA, vomiting, fatigue, poor judgement 40-50 confusion, syncope, tachycardia, tachypnea 50-60 syncope, seizure, coma 60-70 coma, hypotension, arrhythmias, death >70 rapidly fatal

57. CO Poisoning Evaluation and Management Multiple patients have similar complaints of headache and dizziness Oxygen saturation by pulse oximetry will be falsely normal! Give 100% oxygen! CO poisoning causes a metabolic acidosis No need to correct mild acidosis because shifts the curve to the right Check an ECG Consider hyperbaric oxygen therapy

58. Indications for Hyperbaric Oxygen Syncope Coma CO level > 40% Persistent neurologic disturbances Cardiovascular dysfunction Severe acidosis Pregnancy with CO level > 15% or signs of fetal distress

59. Bites and Stings General Approach Treat anaphylaxis Tetanus prophylaxis Copious irrigation with water Consider x-ray for fracture or foreign body Do not suture contaminated wounds

60. Bites: Cats, Dogs, Humans Infection rates Cats: 40-80% Humans: 20-40% Dogs: 5-10% Delayed primary closure Consider prophylactic antibiotics, rabies shots Special cases Cat-scratch disease “ Fight-bite”

61. Scorpion Bites Burning and stinging without visible injury Findings Tachycardia, diaphoresis Roving eye movements Opisthotomos-arched body with head and heels bent back Fasiculations “ tap test” = exquisite tenderness with light tap Treatment Antivenom for systemic symptoms Benzodiazepines for muscle spasms and fasiculations Pain control Severe envenomations (black scorpion) Pancreatitis Respiratory failure Coagulopathy

62. Spiders Brown recluse and Black widow spiders are very uncommon in India Sacred Heart College, Kerala, India Department of Zoology Southindianspiders.com

63. Brown Recluse Dark violin top Delayed pain Ischemic necrosis Hemolysis Loxoscelism N/V, F/C Muscle/joint aches seizures Treatment No antivenom Dapsone Plastic Surgery

64. Black Widow Spider Red hourglass bottom Two small puncture marks Immediate pain N/V/cramps within 1 hour Painful abdominal cramps mimics appendicitis Treatment Benzodiazepines for cramping Calcium gluconate for pain Anti-venin if severe reaction (HTN, resp failure, shock or coma)

65. Snake Bites 238 snake species in India 15,000-20,000 deaths per year in India Twice as likely to die of rabies than snake bite Only 10-15% of venomous bites result in death (most bites are “dry bites” – no venom injected)

66. Snakes! Romulus Whitaker India’s leading herpetologist Venomous snakes “Big Four” Cobra Russell’s Viper Saw-scaled viper Common Krait Fun Fact: Famous King Cobra is &quot;ophiphagus“: they eat only snakes!

67. Cobra Speacle or monocle “hood” makes it easiest to identify Color: cream to black; brown most common Only treatment: anti-venom vaccine

68. Russel Viper Heavy-bodied – resembles small python Narrow necks and triangular heads Chain-like pattern on back Color mostly yellowish and brown Most lethal bite – causes hemorrhaging and nephrotoxicity Requires large amounts of anti-venom vaccine #1 cause of acute renal failure in a few small Asian countries

69. Common Krait Color: blue-black Shiny Transverse thin white crossbands Venom is extremely toxic – induces nerve paralysis Not aggressive and inactive during the daytime

70. Saw Scaled Viper Triangular head typical of the viper Brownish with white markings Chain-like pattern common Smallest of the “big four” - about 1 foot in length Bite rarely fatal because small venom quantity