Maulana Azad Medical College , profile picture
Uploaded byMaulana Azad Medical College
PPTX, PDF1,890 views

Hyperthermia and heat stroke

Hyperthermia and heat stroke are conditions caused by the body failing to regulate its core temperature. Hyperthermia occurs when the body gains too much heat or loses too little, while fever is a regulated increase in temperature by the hypothalamus in response to infection. Heat illnesses form a spectrum from mild heat cramps to the most severe, heat stroke, defined as a core temperature over 40°C with neurological dysfunction. Heat stroke results from a failure of thermoregulation during heat exposure that leads to systemic inflammatory response and multi-organ damage.

Embed presentation

Downloaded 57 times
1 / 103
2 / 103
3 / 103
4 / 103
5 / 103
6 / 103
7 / 103
8 / 103
9 / 103
10 / 103
11 / 103
12 / 103
13 / 103
14 / 103
15 / 103
16 / 103
17 / 103
18 / 103
19 / 103
20 / 103
21 / 103
22 / 103
23 / 103
24 / 103
25 / 103
26 / 103
27 / 103
28 / 103
29 / 103
30 / 103
31 / 103
32 / 103
33 / 103
34 / 103
35 / 103
36 / 103
Most read
37 / 103
38 / 103
39 / 103
40 / 103
41 / 103
42 / 103
43 / 103
44 / 103
Most read
45 / 103
46 / 103
47 / 103
48 / 103
49 / 103
50 / 103
51 / 103
52 / 103
53 / 103
54 / 103
55 / 103
Most read
56 / 103
57 / 103
58 / 103
59 / 103
60 / 103
61 / 103
62 / 103
63 / 103
64 / 103
65 / 103
66 / 103
67 / 103
68 / 103
69 / 103
70 / 103
71 / 103
72 / 103
73 / 103
74 / 103
75 / 103
76 / 103
77 / 103
78 / 103
79 / 103
80 / 103
81 / 103
82 / 103
83 / 103
84 / 103
85 / 103
86 / 103
87 / 103
88 / 103
89 / 103
90 / 103
91 / 103
92 / 103
93 / 103
94 / 103
95 / 103
96 / 103
97 / 103
98 / 103
99 / 103
100 / 103
101 / 103
102 / 103
103 / 103
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 Google to download, for any copyright issues please contact- deepakk70@gmail.com, we will immediately remove it.
HYPERTHERMIA • Rise in body temp. beyond the hypothalamic set point • Due to inadequate loss and/or excessive heat gain. • Failed Thermoregulation.
• What is Fever? • How it is different from Hyperthermia? To Differentiate, Lets first understand the Patho- physiology of both.
PHYSIOLOGY OF THERMOREGULATION
• THERMORECEPTORS IN CORTEX /HYPOTHALAMUS/MID BRAIN/MEDULLA/SC/D EEP ABDOMINAL ORGANS CORE TEMP. • THERMORECEP TORS IN SKIN SHELL TEMP. LAT. SPINOTH ALAMIC TRACT TEMP. CHANGE SENSED TEMP DIFF. FROM SET POINT PREOPTIC /ANTERIOR HYPOTHAL AMOUS THERMOREG ULATION Thermoregulatory center McAllen RM. Preoptic thermoregulatory mechanisms in detail. Am J Physiol Regul Integr Comp Physiol 2004;287(2):R272-3
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
INFECTION/MICROBIA L TOXIN//IMMUNE REACTIONS MONOCYTES/MACROPHA GES/ENDOTHILAIAL CELLS PYROGENIC CYTOKINES(IL-1,IL- 6,TNF,IFN) &MICROBIAL TOXINS HYPOTHALAMIC ENDOTHELIUM PG E2CYCLIC AMP ELEVATED THERMOREGULATORY SET POINT HEAT PRODUCTION &HEAT CONSERAVATION FEVER
HEAT LOSS HEAT GAIN PHYSICAL ACTIVITY BASAL METABOLISM EMOTIONAL/HORMONAL PASSIVE HEAT CONDUCTION(3%) CONVECTION (12-15%) EVAPORATION(25%) RADIATION(55-65%) HYPER THERMIA Lee-Chiong TL Jr, Stitt JT. Disorders of temperature regulation. Compr Ther 1995;21(12):697-704
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
CELLULAR RESPONSE: COMPENSATED (HEAT ILLNESS) SYSTEMIC INFLAMMATORY RESPONSE  LEVELS OF TNF- / IL-1/ IL-6 LEUKOCYTES/ENDOTHELIAL CELLS/EPITHELIAL CELLS CYTOKINES CELL HEALING & REPAIR MODS PREVENTED CELL SURVIVAL RESPONSE HEAT STRESS HEAT SHOCK ELEMENTS  TRANSCRIPTION OF HEAT SHOCK PROTEINS HSP= MOLECULAR CHAPERONES  PREVENT PROTEIN DENATURATION HSP ALSO MODULATE BARORECEPTOR REFELXPREVENT HYPOTENSION
CELLULAR RESPONSE:DECOMPENSATED (HEAT STROKE) • 41-42 deg C TISSUE INJURY IN 1-8 HOURS • DEHYDRATIONHYPOVOLEMIA  SWEATING + CUTANEOUS VASOCONSTRICTION TEMPERATURE • PROINFLAMMATORY MEDIATORS (TNF- /IL- 1/IFN-) DOMINATE OVER ANTI- INFLAMMATORY MEDIATORS ( IL-10 / sTNF- ) • SIR  MODS EXAGGERATED SIR •  EXPRESSION OF ADHESION MOLECULES PROYHROMBOTIC STATE •  AT-3/ PROT C/ PROT S ACTIVATION OF COAGULATION CASCADE • ADVANCED AGE/ FAILURE TO ACCLIMATIZE/GENETIC INADEQUATE HSP RESPONSE • TRANSLOCATION OF ENDOTOXINS & RELEASE OF PRO INFLAMMATORY CYTOKINES  • ENDOTHELIAL ACTIVATIONNO & ENDOTHELIN RELEASE  ALTER HEMODYNAMICS GI ISCHEMIA
HYPERTHERMIA
CHILDREN MORE PRONE TO HYPERTHERMIA GREATER BSA/MASS RATIO MORE HEAT PRODUCED PER KG BWT SLOWER SWEATING RATE SWEATING STARTS AT HIGHER TEMP LOWER CARDIAC OUTPUT Bytomski, Jeffrey R., and Deborah L. Squire. “Heat illness in children..” Current Sports Medicine Reports 2, no. 6 (December 2003)
MECHANISMS AND CAUSES MECHANISMS OF HYPERTHERMIA EXOGENOUS MECHANISMS  HEAT ABSORPTION  HEAT LOSS ENDOGENOUS MECAHNISMS  HEAT PRODUCTION  HEAT LOSS
INCREASED EXOGENOUS HEAT ABSORPTION HOT CLIMATE HOT WORKSHOPS DARK CLOTHING “FORGOTTEN BABY SYNDROME”
EXOGENOUS HEAT ABSORPTIO N
DECREASED EXOGENOUS HEAT LOSS HEAT INSULATING CLOTHING MATERIALS PROTECTIVE EQUIPMENTS/ UNIFORMS HIGH HUMIDIDTY INSUFFICIENT VENTILATION REDUCED WIND
DECREASED HEAT LOSS
ENDOGENOUS INCREASED HEAT PRODUCTION INTENSIVE MUSCULAR LOADING(EXERCISE) PATHOLOGICAL CONTRACTIVE THERMOGENESIS OXIDATION- PHOSPHORYLATIO N DISCONNECTION (2,4 DNP /SALICYLATE/HYPERTHYROI DISM) AUTONOMIC DYSFUNCTION(S S/SYMPATHOMI METIC)
ENDOGENOUS HEAT PRODUCTION
DECREASED ENDOGENOS HEAT LOSS DECREASED SWEAT PRODUCTION (ANTICHOLINERGI C) SKIN VESSEL SPASM(ADENOMIMETICS)
COMMONLY USED ANTICHOLINERGIC DRUGS • Atropine • Hyoscine • Glycopyrrolate • trihexyphenidyl ADRENOMIMETIC DRUGS • theophylline • Caffeine • Ketamine • Ephedrine • Amphetamines
HEAT ILLNESSES
DISEASE SPECTRUM 1. HEAT CRAMPS 2.PRICLY HEAT 3.HEAT TETANY 4.HEAT EXHAUTION 5.HEAT SYNCOPE 6.HEAT EDEMA MOST SEVERE FORM 7. HEAT STROKE
1. 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
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
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
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
• 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
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
Redrawn from Glazer JL: Management of heatstroke and heat exhaustion, American Family Physician
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.
• MANAGEMENT Vital signs + core temp monitoring. Monitoring core temperature- rectal.
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.
Rectal and Esophageal thermometers
• 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
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
HYPERTHERMIA SYNDROMES
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 )
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
NEUROLEPT MALIGNANT SYNDROME 4 cardinal signs – 1. muscle rigidity 2. mental status change(confusion/ catatonia/ bradykinesia/ encephalopathy/ coma) 3. Hyperthermia 4. autonomic instability (labile hypertension /diaphoresis) Neuroleptic agents - Haloperidol/ Chlorpromazine/ Fluphenazine/ Risperidone/ Clozapine/ Olanzapine) • Promethazine and Metoclopramide are also implicated.
DOPAMINE BLOCKADE In hypothalamus alters central thermoregulati on In basal ganglia  muscle rigidity  increased heat production In central mesolimbic regions  altered mental status At level of spinal cord  dysautonomia
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
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.
HEAT STROKE
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
Features Bauchama Misset Pease JAAM Modified JAAM Tempera ture > 40˚C >40.5° C >40.6 °C High environmental temperature High environmental temperature CNS Encephalop athy delirium, convulsions & coma Alteration of mental status (coma, delirium, disorientati on 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
Classification • Classic / Non-Exertional Heat Stroke. • Exertional Heat Stroke.
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)
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
Deaths in India
Deaths due to significant heat waves worldwide
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)
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 %.
• 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
HEAT STROKE SIR MOD DIC
Clinical features • History of Heat exposure/physical exertion • Multi-system involvement- • CNS Irritability, delirium, encephalopathy, coma. • GIT Nausea, Vomiting, Pain Abdomen, Jaundice, melena
CVS • Tachyarrhythmias and hypotension are common. Respiratory • Tachypnea, Distress, Hemoptosis (Edema, ALI, ARDS) Hematological • Rashes, Bleed from various sites (Consump. Caugulopathy and Liver Failure)
Symptoms Kaleiselvan(% symptomatic) Lakhotia Argaud et al. No. Age 26 53+/- 22 102.7+/-2.7 40 42 +/-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%
Close Differentials • CNS- Meningitis, Encephalitis • Infection- Sepsis, Malaria • Grave Disease, Thyroid storm • Drug withdrawals- Narcotics, Benzodiazepines
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
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
Coagulation studies Elevated PT-INR, APTT (DIC) Creatinine kinase Raised (Muscle injury) Chest X ray ARDS Neuroimaging Cerebral infarction, hemorrhage, or edema ECG Arrhythmias
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
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
TREATMENT
PRINCIPLES • FIRST COOL THEN SHIFT • RAPID COOLING METHOD HAS TO BE USED • INTENSIVE CARE UNIT • MOD MONITORING AND ORGAN SPECIFIC TREATMENT
• 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)
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
External cooling methods
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
TEMP MONITOR EQUIPMENT /DRUGSHOLDING BODY HOLDING NECK VITALS MONITOR
?? 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
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
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
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
Combined Ice pack+ evaporation+ fan • Rate of cooling – 0.175 C/m
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
Body Cooling Unit
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.
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
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 H1 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.
Intravascular balloon-catheter system
Extracorporeal Cooling
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.
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
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.
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
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
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
Step 4 • Seek and trace investigation results • Look for signs of coagulopathies, AKI and liver dysfunction • ABG regularly – look for metabolic acidosis • Most important!!!!
Inform / communicate with attendant regarding patient condition
Prevention
THANKS

More Related Content

PPTX
Heat emergencies
byDr.Ashutosh Kumar Singh
 
PDF
.Heat stroke
byHisham Aldabagh
 
PPTX
Heat stroke
bygovernment hospital
 
PPTX
Heat stroke
byMahmoud Ahmad
 
PPT
Heat stroke and its managemnets
byRuhul Amin
 
PPTX
Hyperthermia and hypothermia
bySCGH ED CME
 
PDF
Heat stroke and rhabdomyolysis 2017 final
byCHAKEN MANIYAN
 
PPT
heat 1. heat and related illness ppt.ppt
bybasawantraopatil1
 
Heat emergencies
byDr.Ashutosh Kumar Singh
 
.Heat stroke
byHisham Aldabagh
 
Heat stroke
bygovernment hospital
 
Heat stroke
byMahmoud Ahmad
 
Heat stroke and its managemnets
byRuhul Amin
 
Hyperthermia and hypothermia
bySCGH ED CME
 
Heat stroke and rhabdomyolysis 2017 final
byCHAKEN MANIYAN
 
heat 1. heat and related illness ppt.ppt
bybasawantraopatil1
 

What's hot

PPTX
heat stroke
bySrirama Anjaneyulu
 
PPTX
ARTERIAL BLOOD GASES INTERPRETATION
byDr.RMLIMS lucknow
 
PPT
Hypothermia
byfathi neana
 
PPT
An approach to an unconscious patient
byMontasir Ahmed
 
PPT
Hyperthermia
byvetdrfahadriaz
 
PPTX
Anaphylaxis
byVirendra Hindustani
 
PPTX
Electrolytes abnormalities
byAftab Siddiqui
 
PPTX
systemic inflammatory response syndrome (SIRS)
byNilesh Kucha
 
PPTX
Hyperkalemia
byAMRUTHA JOSE
 
PPTX
ABG Interpretation
byGarima Aggarwal
 
PPTX
Anaphylaxis
bymoduledesign
 
PPT
Acute left ventricular failure
byPROFESSOR DR. MD. TOUFIQUR RAHMAN
 
PPTX
Hyperthermia
byJasmine John
 
PPTX
Management of diabetic ketoacidosis
byNgọc Anh Lương
 
PDF
6 acls
byBác sĩ nhà quê
 
DOC
Apical impulse
byKurian Joseph
 
PPTX
Approach to a patient in shock
byAnkur Kaushik
 
PPTX
Acute Severe Asthma.pptx
byEmmanuelNimrod
 
PPTX
Diagnosis &amp; management of status asthmaticus
bySheela Aglecha
 
PPT
DIABETIC KETOACIDOSIS GUIDELINES
byDr. Darayus P. Gazder
 
heat stroke
bySrirama Anjaneyulu
 
ARTERIAL BLOOD GASES INTERPRETATION
byDr.RMLIMS lucknow
 
Hypothermia
byfathi neana
 
An approach to an unconscious patient
byMontasir Ahmed
 
Hyperthermia
byvetdrfahadriaz
 
Anaphylaxis
byVirendra Hindustani
 
Electrolytes abnormalities
byAftab Siddiqui
 
systemic inflammatory response syndrome (SIRS)
byNilesh Kucha
 
Hyperkalemia
byAMRUTHA JOSE
 
ABG Interpretation
byGarima Aggarwal
 
Anaphylaxis
bymoduledesign
 
Acute left ventricular failure
byPROFESSOR DR. MD. TOUFIQUR RAHMAN
 
Hyperthermia
byJasmine John
 
Management of diabetic ketoacidosis
byNgọc Anh Lương
 
6 acls
byBác sĩ nhà quê
 
Apical impulse
byKurian Joseph
 
Approach to a patient in shock
byAnkur Kaushik
 
Acute Severe Asthma.pptx
byEmmanuelNimrod
 
Diagnosis &amp; management of status asthmaticus
bySheela Aglecha
 
DIABETIC KETOACIDOSIS GUIDELINES
byDr. Darayus P. Gazder
 

Similar to Hyperthermia and heat stroke

PPTX
heat stroke.pptx by sms mc jaipur Rajasthan
bydineshdandia
 
PPTX
Temperature regulation disorders
byAneesh Bhandary
 
PPTX
Heat illnesses in children
byAnitha Edara
 
PPTX
Neurology of heat stroke
bySrirama Anjaneyulu
 
PPT
20161011092733102.ppt
bysjamsulbahri3
 
PPTX
Heat related illnesses
byVyjayanthi Kadambi
 
PPTX
HEAT RELATED ILLNESSES.pptx sms medical college
bydineshdandia
 
PPTX
Heat emergencies(Emergency Medicine)
bykalyan ram
 
PPTX
Heat-Related Illnesses - Dr A B KGMOA.pptx
byThejusSurendran
 
PPTX
A CME on Heat Emergency - A case scenario
byNgYuXuan1
 
PPTX
Heat-Related Illnesses lecture 2024,Power point
byAli Awas
 
PPTX
Heat related illness
bySCGH ED CME
 
PPTX
Alterations in body temperature
byRuppaMercy
 
PPT
Thermoregulation pathophysiology and FUO work up
byGraikosKonstantinos
 
PDF
Body Temperture an other special one in physiology.
byCabdallaQardhaas
 
PPTX
heat stroke and heat exhaustion in children
bySumeraAhmad5
 
PPTX
HEAT RELATED ILLNESSES - update and management
byanjali909chanyal
 
PPTX
Vital signs. Body Temperature Pulse Rate (Heart Rate) Respiration R...
byDelphyVarghese
 
PPTX
Clinical management of heat related illness, moh
byLee Oi Wah
 
PPTX
Dr. pom (2)
byLeahBrady8
 
heat stroke.pptx by sms mc jaipur Rajasthan
bydineshdandia
 
Temperature regulation disorders
byAneesh Bhandary
 
Heat illnesses in children
byAnitha Edara
 
Neurology of heat stroke
bySrirama Anjaneyulu
 
20161011092733102.ppt
bysjamsulbahri3
 
Heat related illnesses
byVyjayanthi Kadambi
 
HEAT RELATED ILLNESSES.pptx sms medical college
bydineshdandia
 
Heat emergencies(Emergency Medicine)
bykalyan ram
 
Heat-Related Illnesses - Dr A B KGMOA.pptx
byThejusSurendran
 
A CME on Heat Emergency - A case scenario
byNgYuXuan1
 
Heat-Related Illnesses lecture 2024,Power point
byAli Awas
 
Heat related illness
bySCGH ED CME
 
Alterations in body temperature
byRuppaMercy
 
Thermoregulation pathophysiology and FUO work up
byGraikosKonstantinos
 
Body Temperture an other special one in physiology.
byCabdallaQardhaas
 
heat stroke and heat exhaustion in children
bySumeraAhmad5
 
HEAT RELATED ILLNESSES - update and management
byanjali909chanyal
 
Vital signs. Body Temperature Pulse Rate (Heart Rate) Respiration R...
byDelphyVarghese
 
Clinical management of heat related illness, moh
byLee Oi Wah
 
Dr. pom (2)
byLeahBrady8
 

More from Maulana Azad Medical College

PPTX
Common sleep disorders in children
byMaulana Azad Medical College
 
PPTX
Childhood Interstitial lung disease (ILD)
byMaulana Azad Medical College
 
PPTX
Pediatric pulmonary function tests
byMaulana Azad Medical College
 
PPTX
Chest xrays
byMaulana Azad Medical College
 
PPTX
Tropical diseases in India.
byMaulana Azad Medical College
 
PPTX
Growth assesment in children
byMaulana Azad Medical College
 
PPTX
Management of chronic asthma Pediatrics
byMaulana Azad Medical College
 
PPTX
Coronavirus
byMaulana Azad Medical College
 
PPTX
Pediatric Bronchial Asthma
byMaulana Azad Medical College
 
PPTX
Tb meningitis and neurocysticercosis
byMaulana Azad Medical College
 
PPTX
Approach to a child with respiratory distress
byMaulana Azad Medical College
 
Common sleep disorders in children
byMaulana Azad Medical College
 
Childhood Interstitial lung disease (ILD)
byMaulana Azad Medical College
 
Pediatric pulmonary function tests
byMaulana Azad Medical College
 
Chest xrays
byMaulana Azad Medical College
 
Tropical diseases in India.
byMaulana Azad Medical College
 
Growth assesment in children
byMaulana Azad Medical College
 
Management of chronic asthma Pediatrics
byMaulana Azad Medical College
 
Coronavirus
byMaulana Azad Medical College
 
Pediatric Bronchial Asthma
byMaulana Azad Medical College
 
Tb meningitis and neurocysticercosis
byMaulana Azad Medical College
 
Approach to a child with respiratory distress
byMaulana Azad Medical College
 

Recently uploaded

PDF
Early Warning Signs of Brain Tumors - Atlantic Brain and Spine
byAtlantic Brain and Spine
 
PDF
Best Nonprofit Medical Cost Sharing for Preventive Services
byZion HealthShare
 
PPTX
Cholestasis-Syndrome-in-Acute-Viral-Hepatitis-An-Overview.pptx
bydiyapadhiyar30
 
PPTX
Think and Grow Rich 2.0 How to future proof your career in the 4th industrial...
byArlen Meyers, MD, MBA
 
PPTX
50 Hrs - Yoga & Dialectical Behaviour Therapy (YDBT) Teacher Training Certifi...
byKaruna Yoga Vidya Peetham
 
PDF
Interoperability in Healthcare systems IH
byAeris seo
 
PPTX
Acute pulmonary edema and its causes .pptx
bymadhusudhanr91
 
PPTX
Physiology of Micturition, Unit 9 Renal System
byKeertis1
 
PDF
Institutional Quality & Accreditation Master Framework to achieve highest NAA...
byDr Jitu Lal Meena
 
PPTX
TB_Prevalevvvbbbbbnn. nnnnnnnnnnnnnnnnpptx
bychandankr9496
 
PPTX
Case study on the malaria disease to mosquito bite
byshankargodve07
 
PDF
1.3 Le Système de Gestion d_une Base de Données.pdf
byMessaoudi Mohamed
 
PPTX
Cardiovascular health.pptx for cardiovascular health
byscionhealthcare
 
PPTX
Yoga for Cancer Teacher Training Program Overview.pptx
byKaruna Yoga Vidya Peetham
 
PPTX
DRUG ESTROGEN FOR NURSING STUDENTS.pptx
bySUDHA GAUTAM
 
PDF
Pediatric ALD (pALD) HCW sensitization slides (1).pdf
byRuth640163
 
PDF
Key Highlights From Recent Dr Ranjit Jagtap News
byDr Ranjit Jagtap
 
PDF
Ocular Health Evaluation with Retinal Imaging (Optomap)
bytylriii07
 
PDF
Why Massages from Rangeela Massage Center Ajman is Essential in 2026
byRangeela Spa Ajman
 
PPTX
Heart Block ppt made by 1sy year NH student
byAfifKhan7
 
Early Warning Signs of Brain Tumors - Atlantic Brain and Spine
byAtlantic Brain and Spine
 
Best Nonprofit Medical Cost Sharing for Preventive Services
byZion HealthShare
 
Cholestasis-Syndrome-in-Acute-Viral-Hepatitis-An-Overview.pptx
bydiyapadhiyar30
 
Think and Grow Rich 2.0 How to future proof your career in the 4th industrial...
byArlen Meyers, MD, MBA
 
50 Hrs - Yoga & Dialectical Behaviour Therapy (YDBT) Teacher Training Certifi...
byKaruna Yoga Vidya Peetham
 
Interoperability in Healthcare systems IH
byAeris seo
 
Acute pulmonary edema and its causes .pptx
bymadhusudhanr91
 
Physiology of Micturition, Unit 9 Renal System
byKeertis1
 
Institutional Quality & Accreditation Master Framework to achieve highest NAA...
byDr Jitu Lal Meena
 
TB_Prevalevvvbbbbbnn. nnnnnnnnnnnnnnnnpptx
bychandankr9496
 
Case study on the malaria disease to mosquito bite
byshankargodve07
 
1.3 Le Système de Gestion d_une Base de Données.pdf
byMessaoudi Mohamed
 
Cardiovascular health.pptx for cardiovascular health
byscionhealthcare
 
Yoga for Cancer Teacher Training Program Overview.pptx
byKaruna Yoga Vidya Peetham
 
DRUG ESTROGEN FOR NURSING STUDENTS.pptx
bySUDHA GAUTAM
 
Pediatric ALD (pALD) HCW sensitization slides (1).pdf
byRuth640163
 
Key Highlights From Recent Dr Ranjit Jagtap News
byDr Ranjit Jagtap
 
Ocular Health Evaluation with Retinal Imaging (Optomap)
bytylriii07
 
Why Massages from Rangeela Massage Center Ajman is Essential in 2026
byRangeela Spa Ajman
 
Heart Block ppt made by 1sy year NH student
byAfifKhan7
 

Hyperthermia and heat stroke

  • 1.
    HYPERTHERMIA AND HEAT STROKE DRDEEPAK KUMAR ASSISTANT PROFESSOR MAULANA AZAD MEDICAL COLLEGE NEW DELHI, INDIA Images used in this PPT are freely available on Google to download, for any copyright issues please contact- deepakk70@gmail.com, we will immediately remove it.
  • 2.
    HYPERTHERMIA • Rise inbody temp. beyond the hypothalamic set point • Due to inadequate loss and/or excessive heat gain. • Failed Thermoregulation.
  • 3.
    • What isFever? • How it is different from Hyperthermia? To Differentiate, Lets first understand the Patho- physiology of both.
  • 4.
  • 5.
    • THERMORECEPTORS IN CORTEX /HYPOTHALAMUS/MID BRAIN/MEDULLA/SC/D EEPABDOMINAL ORGANS CORE TEMP. • THERMORECEP TORS IN SKIN SHELL TEMP. LAT. SPINOTH ALAMIC TRACT TEMP. CHANGE SENSED TEMP DIFF. FROM SET POINT PREOPTIC /ANTERIOR HYPOTHAL AMOUS THERMOREG ULATION Thermoregulatory center McAllen RM. Preoptic thermoregulatory mechanisms in detail. Am J Physiol Regul Integr Comp Physiol 2004;287(2):R272-3
  • 7.
    FEVER • Body’s defensiveresponse • 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
  • 8.
    INFECTION/MICROBIA L TOXIN//IMMUNE REACTIONS MONOCYTES/MACROPHA GES/ENDOTHILAIAL CELLS PYROGENIC CYTOKINES(IL-1,IL- 6,TNF,IFN) &MICROBIALTOXINS HYPOTHALAMIC ENDOTHELIUM PG E2CYCLIC AMP ELEVATED THERMOREGULATORY SET POINT HEAT PRODUCTION &HEAT CONSERAVATION FEVER
  • 9.
    HEAT LOSS HEATGAIN PHYSICAL ACTIVITY BASAL METABOLISM EMOTIONAL/HORMONAL PASSIVE HEAT CONDUCTION(3%) CONVECTION (12-15%) EVAPORATION(25%) RADIATION(55-65%) HYPER THERMIA Lee-Chiong TL Jr, Stitt JT. Disorders of temperature regulation. Compr Ther 1995;21(12):697-704
  • 10.
    HYPERTHERMIA VS FEVER HYPERTHERMIAFEVER 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
  • 11.
    CELLULAR RESPONSE: COMPENSATED(HEAT ILLNESS) SYSTEMIC INFLAMMATORY RESPONSE  LEVELS OF TNF- / IL-1/ IL-6 LEUKOCYTES/ENDOTHELIAL CELLS/EPITHELIAL CELLS CYTOKINES CELL HEALING & REPAIR MODS PREVENTED CELL SURVIVAL RESPONSE HEAT STRESS HEAT SHOCK ELEMENTS  TRANSCRIPTION OF HEAT SHOCK PROTEINS HSP= MOLECULAR CHAPERONES  PREVENT PROTEIN DENATURATION HSP ALSO MODULATE BARORECEPTOR REFELXPREVENT HYPOTENSION
  • 12.
    CELLULAR RESPONSE:DECOMPENSATED (HEATSTROKE) • 41-42 deg C TISSUE INJURY IN 1-8 HOURS • DEHYDRATIONHYPOVOLEMIA  SWEATING + CUTANEOUS VASOCONSTRICTION TEMPERATURE • PROINFLAMMATORY MEDIATORS (TNF- /IL- 1/IFN-) DOMINATE OVER ANTI- INFLAMMATORY MEDIATORS ( IL-10 / sTNF- ) • SIR  MODS EXAGGERATED SIR •  EXPRESSION OF ADHESION MOLECULES PROYHROMBOTIC STATE •  AT-3/ PROT C/ PROT S ACTIVATION OF COAGULATION CASCADE • ADVANCED AGE/ FAILURE TO ACCLIMATIZE/GENETIC INADEQUATE HSP RESPONSE • TRANSLOCATION OF ENDOTOXINS & RELEASE OF PRO INFLAMMATORY CYTOKINES  • ENDOTHELIAL ACTIVATIONNO & ENDOTHELIN RELEASE  ALTER HEMODYNAMICS GI ISCHEMIA
  • 13.
  • 14.
    CHILDREN MORE PRONE TO HYPERTHERMIA GREATERBSA/MASS RATIO MORE HEAT PRODUCED PER KG BWT SLOWER SWEATING RATE SWEATING STARTS AT HIGHER TEMP LOWER CARDIAC OUTPUT Bytomski, Jeffrey R., and Deborah L. Squire. “Heat illness in children..” Current Sports Medicine Reports 2, no. 6 (December 2003)
  • 15.
    MECHANISMS AND CAUSES MECHANISMS OF HYPERTHERMIA EXOGENOUS MECHANISMS HEAT ABSORPTION  HEAT LOSS ENDOGENOUS MECAHNISMS  HEAT PRODUCTION  HEAT LOSS
  • 16.
  • 17.
  • 18.
  • 19.
  • 20.
  • 21.
  • 22.
  • 24.
    COMMONLY USED ANTICHOLINERGIC DRUGS • Atropine •Hyoscine • Glycopyrrolate • trihexyphenidyl ADRENOMIMETIC DRUGS • theophylline • Caffeine • Ketamine • Ephedrine • Amphetamines
  • 25.
  • 26.
  • 27.
    1. 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
  • 28.
    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
  • 29.
    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
  • 30.
    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
  • 31.
    • 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
  • 32.
    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
  • 33.
    Redrawn from GlazerJL: Management of heatstroke and heat exhaustion, American Family Physician
  • 34.
    WHEN TO CONSIDERHOSPITALISATION? • 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.
  • 35.
    • MANAGEMENT Vital signs+ core temp monitoring. Monitoring core temperature- rectal.
  • 36.
    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.
  • 37.
  • 38.
    • Laboratory evaluation Eletrolyteimbalances 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
  • 39.
    Seen commonly inelderly 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
  • 40.
  • 41.
    MALIGNANT HYPERTHERMIA • Geneticsyndrome (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 )
  • 42.
    Management • Immediate discontinuationof 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
  • 43.
    NEUROLEPT MALIGNANT SYNDROME 4cardinal signs – 1. muscle rigidity 2. mental status change(confusion/ catatonia/ bradykinesia/ encephalopathy/ coma) 3. Hyperthermia 4. autonomic instability (labile hypertension /diaphoresis) Neuroleptic agents - Haloperidol/ Chlorpromazine/ Fluphenazine/ Risperidone/ Clozapine/ Olanzapine) • Promethazine and Metoclopramide are also implicated.
  • 44.
    DOPAMINE BLOCKADE In hypothalamus alters central thermoregulati on In basalganglia  muscle rigidity  increased heat production In central mesolimbic regions  altered mental status At level of spinal cord  dysautonomia
  • 45.
    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
  • 46.
    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.
  • 47.
  • 48.
    Definition • No universallyaccepted 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
  • 49.
    Features Bauchama MissetPease JAAM Modified JAAM Tempera ture > 40˚C >40.5° C >40.6 °C High environmental temperature High environmental temperature CNS Encephalop athy delirium, convulsions & coma Alteration of mental status (coma, delirium, disorientati on 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
  • 50.
    Classification • Classic /Non-Exertional Heat Stroke. • Exertional Heat Stroke.
  • 51.
    Features Classic heatstroke 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)
  • 52.
    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
  • 53.
  • 54.
    Deaths due tosignificant heat waves worldwide
  • 55.
    Heat Wave • Conditionthat 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)
  • 57.
    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 %.
  • 59.
    • Mortality fromheat 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
  • 60.
  • 61.
    Clinical features • Historyof Heat exposure/physical exertion • Multi-system involvement- • CNS Irritability, delirium, encephalopathy, coma. • GIT Nausea, Vomiting, Pain Abdomen, Jaundice, melena
  • 62.
    CVS • Tachyarrhythmias andhypotension are common. Respiratory • Tachypnea, Distress, Hemoptosis (Edema, ALI, ARDS) Hematological • Rashes, Bleed from various sites (Consump. Caugulopathy and Liver Failure)
  • 63.
    Symptoms Kaleiselvan(% symptomatic) Lakhotia Argaudet al. No. Age 26 53+/- 22 102.7+/-2.7 40 42 +/-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%
  • 64.
    Close Differentials • CNS-Meningitis, Encephalitis • Infection- Sepsis, Malaria • Grave Disease, Thyroid storm • Drug withdrawals- Narcotics, Benzodiazepines
  • 65.
    Laboratory evaluation Test FindingsInterpretation 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
  • 66.
    LFT Elevation inAST 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
  • 67.
    Coagulation studies ElevatedPT-INR, APTT (DIC) Creatinine kinase Raised (Muscle injury) Chest X ray ARDS Neuroimaging Cerebral infarction, hemorrhage, or edema ECG Arrhythmias
  • 68.
    ECG Changes • Seenin 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
  • 69.
    Neuroimaging MRI- • selective vulnerabilityof 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
  • 70.
  • 71.
    PRINCIPLES • FIRST COOLTHEN SHIFT • RAPID COOLING METHOD HAS TO BE USED • INTENSIVE CARE UNIT • MOD MONITORING AND ORGAN SPECIFIC TREATMENT
  • 72.
    • Deaths hasbeen 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)
  • 73.
    COOLING METHODS COOL WATERIMMERSION EXTERNAL COOLING METHODS INTERNAL COOLING METHODS CONDUCTION METHOD EVAPORATION AND FANNING COOL IV SALINE GASTRIC LAVAGE BLADDER/BOWEL IRRIGATION BODY COOLING UNIT
  • 74.
  • 75.
    Whole body coldwater 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
  • 76.
  • 77.
    ?? 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
  • 78.
    Disadvantages • Whole setupis cumbersome • More man power required • Difficult to maintain IV access/vitals monitoring • CPR if needed, cant be performed • Patient can vomit, pass stool/urine
  • 79.
    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
  • 80.
    Cooling by icepacks • 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
  • 83.
    Combined Ice pack+evaporation+ fan • Rate of cooling – 0.175 C/m
  • 84.
    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
  • 85.
  • 86.
    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.
  • 87.
    Internal cooling method Includegastric, 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
  • 88.
    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 H1 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.
  • 89.
  • 90.
  • 91.
    Medications Dantrolene: Impairs calciumrelease 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.
  • 92.
    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
  • 94.
    At site otherthan 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.
  • 95.
    AT HEALTH CENTRE STEP1 • 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
  • 97.
    STEP-2. Initiate coolingprocess • 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
  • 99.
    STEP 3. • Coolingcan 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
  • 100.
    Step 4 • Seekand trace investigation results • Look for signs of coagulopathies, AKI and liver dysfunction • ABG regularly – look for metabolic acidosis • Most important!!!!
  • 101.
    Inform / communicatewith attendant regarding patient condition
  • 102.
  • 103.

Editor's Notes

  • #7 Mechanism how thermoregulation done.
  • #11 Add Hypothalamic set point
  • #12 Read in detail, Cytokines and hsp mechanism
  • #13 We will take this slide to heat stroke
  • #15 ADD SOURCE/REFERENCE Below slide You have to explain every point
  • #22 Background black
  • #28 Mechanism is not clear, add diff diagnosis
  • #29 Add Differential Diagnosis and how to differentiate with others
  • #31 Search more for heat exhaustion, what to monitor, when to hospitalize, treatment PUT IN 2-3 slides.
  • #37 Mean Difference between axillary and rectal- 0.7 C +/- 0.5
  • #42 How to diagnose, decongest the slides, flow diagram or search pic diagram for mechanism
  • #44 Decongest the slides
  • #50 Japanese Ass Acute Medicine
  • #52 Make the table remove medications, cns, ards and acid base
  • #54 CAUSES OF DEATHS IN HEAT WAVE - % OF HEAT RELATED ILLNESS.
  • #55 CRED- Centre for Research on the Epidemiology of Disasters
  • #56 Correct heat wave definition
  • #61 ADD WITH IMAGES
  • #69 AGE GROUP- 32 TO 79 YEARS, MIMISH – 34 PATIENTS, Mean core tmp- 41.7 +/- 0.9, ECG done post cooling.
  • #70 Add table
  • #73 Search slide with time based heat response of body.