Hyperthermia and heat stroke

Complete description including diagnosis and management
Contain both minor and major heat illnesses

1. HYPERTHERMIA AND HEAT STROKE DR DEEPAK KUMAR ASSISTANT PROFESSOR MAULANA AZAD MEDICAL COLLEGE NEW DELHI, INDIA Images used in this PPT are freely available on G oogle to download, for any copyright issues please contact- [email protected] , we will immediately remove it.

2. HYPERTHERMIA Rise in body temp. beyond the hypothalamic set point Due to inadequate loss and/or excessive heat gain. Failed Thermoregulation.

3. What is Fever? How it is different from Hyperthermia? To Differentiate, Lets first understand the Patho -physiology of both.

4. PHYSIOLOGY OF THERMOREGULATION

5. Thermoregulatory center McAllen RM. Preoptic thermoregulatory mechanisms in detail. Am J Physiol Regul Integr Comp Physiol 2004;287(2):R272-3

6. FEVER Body’s defensive response Hypothalamic set point is raised Thermo-regulated elevation of body temp. Unfavourable environment for pathogens to grow High grade >40 C can be seen but remains briefly followed by sweating

7. IMBALANCE HYPER THERMIA Lee- Chiong TL Jr , Stitt JT. Disorders of temperature regulation. Compr Ther 1995;21(12):697-704

8. HYPERTHERMIA VS FEVER HYPERTHERMIA FEVER Setting Environmental exposure/increased production/decreased dissipation Infection Temperature (>40 deg C/104 deg F) common (>40 deg C/104 deg F) rare Hypothalamic set point Not raised raised Sweating Usually absent or minimal but may be present continuously Profuse Skin Dry /flushed Moist Shivering Absent Present Response to antipyretics Absent Marked

9. CELLULAR RESPONSE: COMPENSATED (HEAT ILLNESS)

10. CELLULAR RESPONSE:DECOMPENSATED (HEAT STROKE)

11. HYPERTHERMIA

12. Bytomski , Jeffrey R., and Deborah L. Squire. “Heat illness in children..” Current Sports Medicine Reports 2, no. 6 (December 2003)

13. MECHANISMS AND CAUSES

14. EXOGENOUS HEAT ABSORPTION

15. DECREASED HEAT LOSS

16. ENDOGENOUS HEAT PRODUCTION

17. COMMONLY USED ANTICHOLINERGIC DRUGS Atropine Hyoscine Glycopyrrolate trihexyphenidyl ADRENOMIMETIC DRUGS theophylline Caffeine Ketamine Ephedrine Amphetamines

18. HEAT ILLNESSES

19. MOST SEVERE FORM 7. HEAT STROKE

20. HEAT CRAMPS Intermittent ,painful, spasmodic contraction of skeletal muscles (Calf & hamstring) During / after vigorous exercise Hypotonic fluid + insuff . Na intake  hyponatremia  prevent Na gradient from being strong enough to power the Ca pumps  Ca ions remain in the myofibrils  muscle stays contracted Oral rehydration and electrolyte replenishment

21. 2. PRICKLY HEAT ( MILIRIA RUBRA/SWEAT RASH/HEAT RASH) Macular /popular/vesicular, erythematous, pruritic rash Common @ clothed areas Blockage of sweat gland openings by stratum corneum debris causing inflammation of sweat glands Ducts rupture  vesicles  risk of other major heat illness increase(if large surface of the body involved) due to anhidrosis in the affected region Loose & clean clothes + Antihistaminics

22. 3. HEAT TETANY Heat  hyperventilation  respi alkalosis  parsthesias (extremities & circumoral ) & carpopedal spasm High pH causes enhanced binding of calcium with proteins  iCa Can be differentiated from heat cramps as there is very little to no pain Cooling

23. 4. HEAT EXHAUTION Illness with nonspecific symptoms. Common- General irritability, fatigue, weakness, light-headedness, headache, nausea ,vomiting, and muscle cramps. accompanied by poor judgment, irritability, dizziness, making differentiation from heat stroke difficult. Core temp. < 40 deg C

24. 2 types - water depletion type - lack of fluid intake + exertion in hot environment -signs of hypovolemia predominate salt depletion type - consumption of hypotonic fluids hyponatremia  neurological features  seizures & coma Most cases – mixed salt and water depletion

25. MANAGEMENT Initial management – on site Discontinue motor activity Remove source of heat exposure Reduce clothing or equipment. Shift to a cool or air-conditioned space Place in Supine position  Raise lower extremities slightly  Venous return Oral rehydration therapy

26. Redrawn from Glazer JL: Management of heatstroke and heat exhaustion, American Family Physician

27. WHEN TO CONSIDER HOSPITALISATION? The symptoms of heat exhaustion mostly resolve within 2–3 hours. If- Patient’s symptoms have not improved within the first 20–30 minutes of the initial on site management.

28. MANAGEMENT Vital signs + core temp monitoring. Monitoring core temperature- rectal.

29. Measuring rectal temp. Put petroleum jelly on the bulb end. Lay the child face down and spread the buttocks apart. Insert the bulb end approx. 3 cm past the anal margin. Held for at least 1 minute, or until the temp. stopped rising. Morley CJ. Axillary and rectal temperature measurements in infants. Arch Dis Child. 1992 Jan;67(1):122-5.

30. Rectal and Esophageal thermometers

31. Laboratory evaluation Eletrolyte imbalances Features of dehydration- elevated hematocrit and serum urea. LFT, KFT, VBG- ?? Heat Stroke progression. Intravenous fluid and electrolyte replacement therapy is employed. More aggressive cooling measures not warranted

32. Seen commonly in elderly patients 5 . HEAT EDEMA Dependent extremities Due to cutaneous vasodilation + pooling of interstitial fluid Resolves within few days Diuretics NOT to be given  volume depletion 6. HEAT SYNCOPE prolonged stationary standing / sudden standing after prolonged heat exposure Volume depletion + peripheral vasodilation + decreased vasomotor tone   venous return causing cerebral hypoperfusion Elderly Fluids + cooling+ supine position

33. HYPERTHERMIA SYNDROMES

34. MALIGNANT HYPERTHERMIA Genetic syndrome (50% AD & 50% point mutation) - gene encoding RYR1 ryanodine receptor The incidence of MH reactions ranges from 1:5,000 to 1:50,000. Neuromuscular disorders (muscular dystrophy, myotonia )  high risk First signs- masseter spasm during ET intubation/ increase ETCO2 Imp . in OT/intensive setting Rosenberg, Henry et al. “Malignant hyperthermia.” Orphanet journal of rare diseases )

35. Management Immediate discontinuation of the possible trigger agent. The inspired gas is converted to 100% oxygen at a high flow rate to wash out residual anaesthetic as rapidly as possible . The dantrolene , 2.5 mg/kg IV, is given as rapidly as possible . Cold normal saline, 15 mL/kg, is administered rapidly if the temperature is > 39°C Hyperkalemia

36. NEUROLEPT MALIGNANT SYNDROME 4 cardinal signs – muscle rigidity mental status change(confusion/ catatonia/ bradykinesia / encephalopathy/ coma) Hyperthermia autonomic instability (labile hypertension /diaphoresis) N euroleptic agents - Haloperidol / Chlorpromazine / F luphenazine / R isperidone / Clozapine / O lanzapine ) Promethazine and Metoclopramide are also implicated.

37. SEROTONIN SYNDROME Triad – abnormalities of- 1. mental status (agitation / hypervigilance / delirium) 2. neuromuscular function ( clonus / hyperreflexia ) 3. autonomic function (hyperthermia/ tachycardia/ HTN/ diaphoresis/vomiting diarrhoea) Develops within 24 hrs of drug admin Overstimulation of 5-HT1A and 5-HT2A

38. Management Antidote- Cyproheptadine , a H1 receptor antagonist with nonspecific serotonergic (5-HT1A and 5-HT2A) antagonistic properties. Cyproheptadine (tablet or syrup). Total daily dose of 0.25 mg/kg divided every 6 hours. The maximum daily dose is 12 mg for children 2-6 years and 16 mg for children 7-14 years old.

39. HEAT STROKE

40. Definition No universally accepted definition exists Bouchama’s definition (commonly used) Core body temp. above 40 °C, accompanied by hot dry skin and CNS abnormalities (delirium, convulsions & coma) Form of hyperthermia associated with SIR that leads multi-organ dysfunction, predominantly encephalopathy. Bouchama A, Knochel JP. Heat stroke. N Engl J Med. 2002;346:1978–88

41. Features Bauchama Misset Pease JAAM Modified JAAM Temperature > 40 ˚ C >40.5°C >40.6 °C High environmental temperature High environmental temperature CNS Encephalopathy delirium, convulsions & coma Alteration of mental status (coma, delirium, disorientation or seizures) Impaired consciousness, Japan Coma Scale score of ≥2 , cerebellar symptoms, convulsions, or seizures) Glasgow Coma Scale (GCS) score of ≤14 Sytemic SIR with MOD Hepatic/renal dysfunction Coagulation disorder Creatinine or total bilirubin levels of ≥1.2 mg/dL Skin Hot, dry skin Hot, dry, or flushed skin

42. Classification Classic / Non- Exertional Heat Stroke. Exertional Heat Stroke .

43. Features Classic heat stroke Exertional heat stroke Age group Prepubertal, elderly Post-pubertal and active Occurrence Epidemic (heat waves) Sporadic (any time of year) Activity Sedentary Strenuous Health status Chronically ill Generally healthy Medications Prescribed for chronic illness None/ illicit drugs Mechanism Absorption of environmental heat and poor heat dissipation Excessie heat production, which overwhelms heat-loss Sweating Maybe absent (dry skin) Usually present (wet skin)

44. Epidemiology “Silent disaster” - develops slowly and kills humans and animals nationwide. > 22,000 fatalities in India (1992-2015). In 2015, the country witnessed the fifth deadliest heat wave in history. 2300 deaths – in Andhra pradesh ., Telangana , Punjab, Odisha , Bihar June 2019- 53.96% population exposed to heat waves National Disaster Management Authority. GOI. 2017

45. Deaths in India

46. Deaths due to significant heat waves worldwide

47. Heat Wave Condition that leads to physiological stress and can cause death due to rise in atmospheric temp. World Meteorological Organization Daily max. temp. exceeds the avg. max. temp. of the area by 5° C for 5 consecutive days. Or if the max temp. of any place continues to >45° C consecutively for 2 days. (Costal >40)

48. Heat index / Apparent temperature What the temp. feels like to the body when the humidity is combined with the air temp. When the humidity is high, rate of perspiration decreases and the body feels warmer. Ex- if air temp. is 34°C and relative humidity is 75%, the heat index--how hot it feels--is 49°C. The same effect is reached at just 31°C when the relative humidity is 100 %.

49. Mortality from heat stroke has been reported to increase due to climate change By the 2050s, heat stroke-related deaths are expected to rise by nearly 2.5 times 25-50% mortality even with aggressive care

50. HEAT STROKE SIR MOD DIC

51. Clinical features History of Heat exposure/physical exertion Multi-system involvement- CNS Irritability, delirium, encephalopathy, coma. GIT Nausea, Vomiting, Pain Abdomen, Jaundice, melena

52. CVS Tachyarrhythmias and hypotension are common. Respiratory Tachypnea , Distress, Hemoptosis (Edema, ALI, ARDS) Hematological Rashes, Bleed from various sites ( Consump . Caugulopathy and Liver Failure)

53. Symptoms Kaleiselvan (% symptomatic) Lakhotia Argaud et al . No. Age 26 53+/- 22 102.7 +/-2.7 40 +/-3 102.2 2.5 83 79.6 ± 9.9 106 ± 2.34 CNS Disoriented Drowsy Coma Seizures All 50 11 34 30 All 50 10 36 32 All 56 3.6 GIT Nausea and Vomiting Diarrhea 30 30 15 Resp Failure ( Mech Vent) 26 (100%) 47 (60%) Cardiovascular Shock ( vasopressor ) 23 43 Renal (AKI) 57 34 Hepatic 34 2.4 Hematological 26 3.6 35% 64% 30%

54. Close Differentials CNS- Meningitis, Encephalitis Infection- Sepsis, Malaria Grave Disease, Thyroid storm Drug withdrawals- Narcotics, Benzodiazepines

55. Laboratory evaluation Test Findings Interpretation Blood Leukocytosis Systemic inflammation from (heat-related illness or sepsis) Elevated hematocrit Dehydration Thrombocytopenia, elevation in hyper-segmented neutrophils, and atypical lymphocytes heat injury Electrolytes Hyponatremia Hypernatremia hyperkalemia hyperphosphatemia, and hypocalcemia Loss in sweat Dehydration Muscle damage Glucose Hypoglycemia Fulminant hepatic failure

56. LFT Elevation in AST and ALT Liver dysfunction KFT Deranged KFT AKI Urine Proteins Rhabdomyolysis Myoglobulin Rhabdomyolysis Increased sp. gravity Hypovolemia CSF Nonspecific pleocytosis CSF protein elevated Given in National GUIDE Animal model studies. ABG Metabolic acidosis Respiratory alkalosis Lactic acidosis CNS stimulation- hyperventilaton

57. Coagulation studies Elevated PT-INR, APTT (DIC) Creatinine kinase Raised (Muscle injury) Chest X ray ARDS Neuroimaging Cerebral infarction, hemorrhage, or edema ECG Arrhythmias

58. ECG Changes Seen in 85% of HS patients in one study. sinus tachycardia (43-79%) QT prolongation (61%) Both non-specific and specific ST changes associated with coronary artery territories conduction defects- incomplete and complete RBBB Mimish L. Electrocardiographic findings in heat stroke and exhaustion: A study on Makkah pilgrims. Journal of the Saudi Heart Association. 2012; 24(1): 35-9 12. Akhtar MJ, al- Nozha M, al- Harthi S & Nouh MS. Electrocardiographic abnormalities in patients with heat stroke. Chest. 1993; 104(2): 411-4

59. Neuroimaging MRI- selective vulnerability of cerebellar Purkinje cells to heat-induced injury Ischemia/ Hemmorhage in dentate nuclei, cerebellar hemispheres, cerebellar peduncles, midbrain, thalami, hippocampi , basal ganglia, the splenium , temporo -occipital lobes Cerebral Edema Cerebral atrophy ( Late – after 2 weeks, Progressive) Albukrek D, Bakon M, Moran DS, Faibel M, Epstein Y (1997) Heat- strokeinduced cerebellar atrophy: clinical course, CT and MRI findings. Neuroradiology 39: 195–197 Sudhakar PJ, Al- Hashimi H (2007) Bilateral hippocampal hyperintensities : a new finding in MR imaging of heat stroke. Pediatr Radiol 37: 1289–1291

60. TREATMENT

61. PRINCIPLES FIRST COOL THEN SHIFT RAPID COOLING METHOD HAS TO BE USED INTENSIVE CARE UNIT MOD MONITORING AND ORGAN SPECIFIC TREATMENT

62. Deaths has been seen as early as within 30 minutes of heat stroke onset. start effective cooling method with min. rate of 0.20 C/ min. End point used in large series is 39 C (proven safe)

63. COOLING METHODS COOL WATER IMMERSION EXTERNAL COOLING METHODS INTERNAL COOLING METHODS CONDUCTION METHOD EVAPORATION AND FANNING COOL IV SALINE GASTRIC LAVAGE BLADDER/BOWEL IRRIGATION BODY COOLING UNIT

64. External cooling methods

65. Whole body cold water immersion Most effective method of cooling Rapid rate of cooling Ice used in water (1 C) – 0.35 C/min Cold Water (5 C)- 0.15 C/min Immersion of only torso and legs- 0.25 C/min level of neck- 0.35 C/min hands and legs- 0.15 C/min recommended - National Athletic Trainers’ Association and American College of Sports Medicine

66. TEMP MONITOR EQUIPMENT/DRUGS HOLDING BODY HOLDING NECK VITALS MONITOR

67. ?? Peripheral vasoconstriction Thought previously – immersion of body to cold water – per vasoconstriction and shivering ( heat production) Recent studies shown a) Thermogenesis via shivering occurs in normothermic not hyperthermia. (1) b) if +, do not impede the cooling process (2) 1. Proulx CI, Ducharme MB, Kenny GP. Effect of water temperature on cooling efficiency during hyperthermia in humans. J Appl Physiol. 2003;94(4):1317–1323 2. Casa DJ, McDermott BP, Lee E, Yeargin SW, Armstrong LE, Maresh CM. Cold-water immersion: the gold standard for exertional heat stroke treatment. Exerc Sport Sci Rev. 2007;35(3):141–149

68. Disadvantages Whole setup is cumbersome More man power required Difficult to maintain IV access/vitals monitoring CPR if needed, cant be performed Patient can vomit, pass stool/urine

69. Evaporation and fanning Less efficient c/w cold water immersion Rate of cooling- o.15 C/min Body exposed- mist sprayer filled with cold water is sprayed all over the body- continued with air fan @ min 0.5 m/s. If sprayer is not available, cold towels can be used. Brendon P. McDermott et al. Acute Whole-Body Cooling for Exercise-Induced Hyperthermia: A Systematic Review. Journal of Athletic Training 2009;44(1):84–93

70. Cooling by ice packs Conductive cooling by the application of crushed ice or ice packs to the body strategic application of ice packs to the axilla , neck, and groin Rate of cooling- 0.028 C/m When applied to whole body- 0.034 C/m Ineffective method- takes 110 minutes to cool a patient from 42.2C (108F) to 38.9C (102F) Brendon P. McDermott et al. Acute Whole-Body Cooling for Exercise-Induced Hyperthermia: A Systematic Review. Journal of Athletic Training 2009;44(1):84–93

71. Combined Ice pack+ evaporation+ fan Rate of cooling – 0.175 C/m

72. Body-cooling unit (BCU), Specially constructed device, produces a superior cooling rate of 0.31 ˚ C/min Directing air currents while simultaneously spraying water on patients Cost- 18,000 USD!!! Brendon P. McDermott et al. Acute Whole-Body Cooling for Exercise-Induced Hyperthermia: A Systematic Review. Journal of Athletic Training 2009;44(1):84–93

73. Body Cooling Unit

74. Cold External Environment Bring the patient away from the exposure Preferably to the cool area (ac units) Rate of cooling – 21 C/ 20% humidity- 0.06 32 C/ 20% humidity-0.02 management in an ICU without ac were independently associated with an increased risk of hospital death Misset B et al. Mortality of patients with heatstroke admitted to intensive care units during the 2003 heat wave in France: a national multiple-center risk factor study. Crit Care Med. 2006;34: 1087–92.

75. Internal cooling method Include gastric, peritoneal, and bladder lavage with cold water. Rate of cooling- 0.018 C/min Role not been fully established Can be used along with other methods Brendon P. McDermott et al. Acute Whole-Body Cooling for Exercise-Induced Hyperthermia: A Systematic Review. Journal of Athletic Training 2009;44(1):84–93

76. Other cooling methods Intravascular balloon catheter cooling Rate of cooling - 0.12 C/min Inbuilt thermistor for sensing core body temp and fluid infused change in temp. as small as 0.1°C sensed Hamaya H 1 et al. Successful management of heat stroke associated with multiple-organ dysfunction by active intravascular cooling. Am J Emerg Med.  2015 Jan;33(1):124.

77.  Intravascular balloon-catheter system

78. Extracorporeal Cooling

79. Medications Dantrolene : Impairs calcium release from the sarcoplasmic reticulum Reduces muscle excitation and contraction Studies show no difference in cooling rate, outcome, mortality Antithrombin III, rsThrombomodulin α: To treat coagulopathy ?? No proven studies Eran Hadad et al. Clinical review: Treatment of heat stroke: should dantrolene be considered? Crit Care . 2005; 9(1): 86–91 Hagiwara S et al. Highdose antithrombin III prevents heat stroke by attenuating systemic inflammation in rats. Inflamm Res. 2010;59:511–8.

80. Poor prognostic factors Core temp > 40 C- bad, > 42 C - worst Duration of illness, > 60 min- bad, >90 min – worst Age - > 80 yrs, no pediatric data. Associated Heart disease or Malignancy Anuria , Coma On Diuretic therapy Use of Ionotropes within first 24 hours in ICU Management without Ac in ICU Increased PT, Raised ALT > 1000 Hausfater et al. Prognostic factors in non- exertional heatstroke. Intensive Care Med. 2010;36: 272–80. Misset B et al. Mortality of patients with heatstroke admitted to intensive care units during the 2003 heat wave in France: a national multiple-center risk factor study. Crit Care Med. 2006;34: 1087–92

81. At site other than health center Remove clothing, cool water& fan skin. Place ice packs. Offer cool fluids if alert and able to drink Immediately transfer to nearest health care facility While transferring, cooling has to be contd. Start intravenous fluids.

82. AT HEALTH CENTRE STEP 1 Clinical assessment for CVS, Resp & CNS func . Exclude other D/D. Assess airway and ensure good resp. efforts. Put oxygen, IV lines take samples. Check body core temp. - rectal or esophageal. Send ICU call, start and continue treatment

83. STEP-2. Initiate cooling process Removal of body clothing Use mist fan / air conditioned room / Stand fans Ice packs at groins, neck and axilla , spray cool water Ongoing tepid sponging Lavage with cold saline via NG tube or urinary catheter

84. STEP 3. Cooling can be stopped – 39 C Use Benzodiazepines for seizures. DO NOT use PCM or other NSAIDS. Close monitor- Core temp, BP, 4 hourly Dx , Hourly Urine output, ECG, half hourly GCS

85. Step 4 Seek and trace investigation results Look for signs of coagulopathies , AKI and liver dysfunction ABG regularly – look for metabolic acidosis Most important!!!!

86. Inform / communicate with attendant regarding patient condition

87. Prevention

88. THANKS THANKS