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Environmental Heat Illness Exertional Illness -- The Dog-Days of Summer --

Environmental Heat Illness Exertional Illness -- The Dog-Days of Summer --. Joseph R. Cline, MD, FACEP Associate Professor of Medicine University of Wisconsin Medical School.

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Environmental Heat Illness Exertional Illness -- The Dog-Days of Summer --

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  1. Environmental Heat IllnessExertional Illness-- The Dog-Days of Summer -- Joseph R. Cline, MD, FACEP Associate Professor of Medicine University of Wisconsin Medical School

  2. Chicago – 1995 Heat waveJuly 12 – July 20Daily temps 34o-40oC (93o-104oF)Peak Heat Index on Day 248.3oC (119oF) (94oF, 70% humidity)> 600 excess deaths; >3300 E.D. visits

  3. New York Times-- Sports Desk --August 2, 2001 Heat Kills a Pro Football Player N.F.L. Orders a Training Review Korey Stringer, an offensive tackle for the Minnesota Vikings, died early yesterday, a day after collapsing from heatstroke at the Vikings’ training camp in Mankato, Minn.

  4. Heat Illness-- Global Warming -- • January - June 1998 - warmest 6 month period ever recorded • Each month was the warmest month ever recorded • July 1998 - warmest calendar month ever recorded • Major midwest heat waves with high mortality in 1995, 1999 Trend of warming is certain. The effect on heat illness is uncertain but believed to be most related to climactic variability.

  5. Heat Illness--Discussion overview-- • In-depth review of thermoregulation and environmental conditions • Brief review of the spectrum of minor heat illness from heat cramps --- heat exhaustion • In-depth review of classic and exertional heat stroke • Mortality trends • Pathophysiology and Sequelae • Predisposing conditions • Differential diagnosis • Diagnostic criteria • Treatment • Prevention

  6. Mechanisms of Heat Transfer • Conduction • direct contact • thermal conductivity of water is 32 times that of air • Convection • movement of fluid layer next to the body • Radiation • radiant energy emitted solely due to its temperature • Evaporation • 1 kcal of heat dissipated for each 1.7 ml. sweat

  7. Heat Production • Basal rate 75 kcal/hr • Sitting in sun 150 kcal/hr • Moderate work 300 kcal/hr • Strenuous activity 600 - 900 kcal/hr

  8. Heat Load -- Heat Loss • Solar Heat load 250 kcal/hr • Metabolic heat load_____500 kcal/hr • Total load 750 kcal/hr • If ambient temp = 93 degF, then • sweat requirement = 1.3L to • dissipate

  9. Heat Index

  10. Thermoregulation with Heat Stress Metabolic Heat Load (Exercise) Environmental Heat Load Body heat Core temperature Cutaneous vasodilatation Sweating Heat loss by radiation from skin surface Heat loss by evaporation

  11. ADH release threshold Thirst threshold 280 mOsm/L 295 mOsm/L 42L (nl. TBW) X 280 mOsm = TBW thirst threshold 295 mOsm = 39.9 L = 2.1 L deficit THIRST

  12. Acclimatization • Increase aerobic capacity • increased number of mitochondria/cell • increased muscle glycogen stores • Training at intensity above 50% VO2max provides for 1/2 of acclimatization needs • Increased sweating capacity • lower temperature threshold for vasodilatation • increased volume • Increased aldosterone production • 10 - 25%increase in plasma volume • lower sweat sodium conc. (65 - 5 mEq/L) • increase potassium losses

  13. Cardiac output requirementsin Heat Illness • Cutaneous perfusion increases 5 - 20% • Muscle perfusion increases up to 10 times • Volume contraction • Sweat losses • Intracellular osmotic fluid shift

  14. Heat cramps Heat edema Heat syncope Heat exhaustion Heat stroke Spectrum of Heat Illness

  15. Heat Cramps • First described in 1923 in English coal miners, “miner’s cramps” • Originally believed related to excess water intake • Prospective studies have demonstrated no Na+ concentration or plasma volume differences in ultramarathon runners with or without heat cramps • Newly postulated mechanism of altered spinal neural reflex activity

  16. Heat Syncope Cause: temporary ineffective circulating volume due to: • dependent blood pooling • peripheral vasodilatation Treatment: resolves quickly with assumption of horizontal position; hydration Prevention: avoidance of protracted standing; use of frequent muscle flexion and postural changes; acclimatization

  17. Heat Exhaustion – Exercise Associated Collapse-- Diagnosis -- • Symptoms: fatigue, vertigo, impaired judgment, thirst, nausea, vomiting • Core temperature < 40oC (104oF) • Tachycardia, orthostatic hypotension • Differentiation from heat stroke: • modest temperature elevation (< 40oC) • no coma or seizures • normal liver function

  18. Heat Exhaustion – Exercise Associated Collapse-- Treatment -- • Rest, move to cool environment • Assess temperature • Temp(R) > 39oC (103oF) • Temp(R) < 39oC, water sprinkling, ice packs • Assess hydration • BP, pulse, orthostatic V.S., electrolytes • Hydration • Initial (oral): 1 - 2 L over 2 - 4 hrs. • later (oral): 500cc./lb. lost • IV therapy - Saline • Many cases are managed with oral hydration without Emergency department visit

  19. Heat Stroke Predisposing conditions, Differential diagnosis, Diagnostic Criteria, Treatment

  20. Heat Stroke-- Mortality -- • Heat wave years 1952-1955, 1966: average 820 annual U.S. heat stroke deaths • 1979 - 1997 • average of 371 deaths/year in U.S. (.18 / 100,000) • average of 6.6 deaths/year in WI • 1995 Heat wave - 81 heat stroke deaths in WI • Mortality 20% in patients age < 50 yrs. • Overall mortality 10% • Prior to 1950, mortality 40 - 50%

  21. Chicago – 1995 Heat wave Damatte, et al Annals of Internal Medicine, Aug 1998 (1995 Chicago Heat Wave: >600 deaths) • Observational study of 58 critical care patients in 12 hospitals; exertional heat stroke patients excluded • 60 % mechanical ventilation • In-hospital mortality of 21% • Additional mortality of 28% after 1 year • Severe functional impairment at discharge – 33% • > 50% had moderate-severe renal insufficiency • 45% had evidence of D.I.C. • Only 1 / 58 patients cooled to < 38.9oC within 30 minutes with CT scanning a delay factor

  22. Chicago – 1995 Heat wave • 83% of victims found at home • > 80% had medical insurance • 90% had chronic medical conditions • Hypertension • Alcohol abuse • 26% on diuretics • 24% discharged with no neuro impairment • 43% discharged with minimal impairment • 33% discharged with severe neurologic impairment

  23. Hyperthermia--Differential diagnosis--(Non-infectious CNS dysfunction) • Status epilepticus • Malignant hyerthermia • Neuroleptic Malignant Syndrome • Thyroid storm • Hypothalamic stroke • Delirium tremens • Drug induced heat stroke • Parkinson’s Disease

  24. Toxic-mediated Hyperthermia • CNS mediated muscle hypertonicity • Cocaine, PCP, MDMA, Amphetamines, Ephedra • Autonomic effects • Anticholinergics • Tricyclic antidepressants • Oxidative uncoupling • Salicylates • Withdrawl states • Increased basal metabolic rate - endocrine mediated

  25. Malignant Hyperthermia • Abnormal efflux of Ca++ from sarcoplasmic reticulum • ATP-dependent sarcoplasmic retic. Ca++ uptake • myoplasmic Ca++ diffuse muscle contraction and rigidity

  26. Neuroleptic Malignant Syndrome • Extrapyramidal motor dysfunction (rigidity) • Altered thermoregulation (fever) • Autonomic dysfunction • tachycardia • labile blood pressure • diaphoresis

  27. Major criteria fever rigidity increased CK Minor criteria tachycardia labile BP tachypnea altered M.D. diaphoresis leukocytosis Neuroleptic Malignant Syndrome • Mortality: 20% • Incidence: 0.5% - 1% of patients treated with • neuroleptic medications • Diagnosis: 3 Major or 2 Major + 4 minor

  28. “Classic” Heat Stroke -- A combination of circumstances -- Humidity 70% 95oF • Pre-morbid • conditions • Cardiac disease • Diabetes • Parkinson’s Disease • “Total care” patient • Predisposing medications • Phenothiazines • Anticholinergics • Diuretics

  29. Heat Stroke-- Diagnostic Criteria -- • Signs • Temperature > 41oC • Profound CNS signs (coma, delirium, seizure) • Hot, dry skin (sweating persists in 50%) • Must assume Heat Stroke with CNS dysfunction during periods of high environmental temperatures

  30. Classic Heat Stroke Exertional Heat Stroke Age Health status Activity Drug use Sweating Lactic acidosis Rhabdomyalysis Acute renal failure Hypocalcemia DIC CPK Hypoglycemia Mechanism Elderly Chronic illness Sedentary Anticholinergics, diuretics, Antipsychotics, antihypertensives Antidepressants Usually absent Usually absent; poor prognosis if present Unusual < 5% of patients Uncommon Mild Mildly elevated Uncommon Poor dissipation of environmental heat Men (15 - 45yrs) Healthy Strenuous exercise Usually no meds Often present Common; may be marked Frequently severe 25-30% of patients Common Marked Markedly elevated Common Excessive endogenous heat production From Knochel et al: Disorders of heat regulation. In Kleeman et al. Clinical disorders of fluid and electrolyte metabolism, New York, 1987, McGraw-Hill

  31. Pathophysiology of Heat Stroke-- Systemic Considerations -- Skin temp Skin blood flow Compensatory splanchnic vasoconstriction Venous pooling Decreased venous return Compensatory tachycardia Further venous pooling Hypotension Heat storage Cutaneous vasoconstriction

  32. Heat Stroke-- Causes of Shock -- • Hypodynamic variety - myocardial depression and / or volume depletion • Hyperdynamic - severe peripheral vasodilatation

  33. Heat Stroke-- Causes of renal failure -- • Myoglobin converted to nephrotoxic ferrihemate with acidity • Urine dipstick has false negatives; check the CPK • Rhabdomyolysis alone may produce elevated creatinine • Urate crystals from metabolism

  34. Heat Stroke-- Coagulopathy and D.I.C. -- Results from direct thermal injury of vascular endothelium • vascular permeability • expression of adhesion molecules (ICAM-1, vWF, E-selectin, L-selectin • coagulation • protein C,S • antithrombin III • fibrinolysis • Strong correlation between D.I.C. and subsequent A.R.D.S.

  35. Heat Stroke-- Causes of Brain Injury -- • Cerebral edema • Diffuse petechial hemorrhages • Status epilepticus

  36. Heat Stroke - Multisystem Sequelae Ambient temp Prolonged sweating Anticholinergic meds Seizures Exercise K+ Vasodilatation Fluid losses Muscular hyperactivity Muscle perfusion Shock Sweating ceases Rhabdo myolysis Acidosis Further core temp Myoglo- binuria K+ DIC Acute renal failure CNS damage Myocardial injury Arrhythmias

  37. Heat Stroke-- Treatment -- Underlying principle: Prognosis related to speed of cooling to < 39oC • Cooling modalities: Cold water immersion vs. evaporative • Fluid requirements may be modest, depending on “classic” vs exertional • Alpha adrenergic drugs to be avoided • Consider mannitol and/or urinary alkalization • Shivering preferentially treated with benzodiazepine • Seizures are catastrophic complication

  38. Heat Stroke-- Controversy in Cooling Modalities -- Cold water immersion criticized on theoretical concerns of vasoconstriction and shivering Rebuttal: • Immersion induced peripheral vasoconstriction has not been demonstrated • Shivering is not a recognized complication • Thermoregulatory response to heat is 90% dependent on core temp, 10% on skin temp

  39. Heat Stroke-- Cooling strategies -- • Completely undress • Finely atomized tepid water spray • Large fans for convective air currents • Ice packs to neck, axilla and groin • Standard temperature IV fluids • Treat shivering with benzodiazepines • Goal: 38.5 oC within 45 minutes

  40. Heat Stroke-- Treatment -- • ABC’s • Cooling to < 39oC (102.2oF) • Evaporative cooling is preferred • Mortality is directly related to duration of hyperthermia • Avoid overzealous fluid administration • Alpha-adrenergic hemodynamic support to be avoided until normo-thermia achieved • Mannitol and urinary alkalinization

  41. Heat Stroke-- Prevention -- Exertional • Awareness of environmental conditions • Scheduled, required fluid intake (8-12 oz. every 20-30 minutes • Monitoring of pre/post exertional dry weights is recommended

  42. Heat Stroke-- Prevention -- Non-exertional (Classic) • Recognition of environmental predisposing conditions • Recognition of predisposing medications and medical conditions • Liberalization of fluid restrictions when there is no air conditioning • Encourage frequent bathing/showering

  43. Exertional Illness • Exertional Heat Stroke • Exertional Hyponatremia • Exercise Associated Collapse

  44. Exertional Illness--Energy use and Weight loss-- • 2.7 grams of water are complexed to each gram of glycogen stored • Liver contains 100 gram glycogen • Muscle contains 375 gram glycogen • Glycogen-complexed water = 1280 gram • Metabolic water production = 1 gram / gram glycogen • For approximately 500 gram glycogen burned there is 1.7 kg metabolic water loss

  45. 2nd Boom of Running • 1970’s – world-wide fitness movement; expansion of the “big city” marathons • 1990’s – “running tourism”, “charitable cause running”

  46. 2nd Boom of Running Boston 1975 New York City, 1978 New York City, 2001 Men’s winning time 2:09:55 2:12:11 2:07:43 Total no. finishers 1818 8588 23,651 < 3hr 48.8% 9.4% 2.4% 3 - 3.5hr 51.2% 21.1% 8.4% 3.5 - 4hr 29.3% 19.4% 4 - 4.5hr 21.0% 24.4% 4.5 - 5hr 12.2% 22.4% 5 - 5.5hr 5.1% 11.9% 5.5 - 6hr 1.5% 6.1% 6 - 6.5hr 0.4% 2.6% 6.5 - 7hr 0.03% 1.4% 7 - 7.5hr 0.05% 0.6% 7.5 - 8hr 0.3% 8 - 8.5hr 0.1%

  47. Exertional Heat Stroke • Athletes or heavy laborers • Heat production exceeds dissipation Maximal energy expenditure Temperature, Humidity, Convective air current Mass + intensity • Hydration is not a major factor

  48. Exertional Hyponatremia • Incidence – variable; prior to 2000, only 1 reported case in literature • Signs • Nausea, vomiting, headache, altered M.S., potentially seizures • Associations • Less trained runners • Longer finish times • Increased fluid ingestion • Women are more prone

  49. Exertional Hyponatremia Pre-2003 hydration recommendations 1970’s – research suggested dehydration was the greatest risk; exercise associated collapse believed related to dehydration-induced heat illness Recommendations of the 2nd boom “drink until your urine is clear” “don’t wait until you are thirsty to drink”

  50. Exertional Hyponatremia 2003 Hydration recommendations from Position Statement of the International Marathon Medical Directors Association Due to increased reports of exertional hyponatremia • Do not encourage slower runners to drink as much as possible • There is no single recommended amount to drink • Diagnosis of heat illness must have clear evidence of heatstroke • EAC at the finish is much more likely to be due to postural hypotension • Runners should be advised to drink ad libitum (400-800 ml / hr)

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