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CASE PRESENTATION 
NIDA EILY 
PGR WEST MEDICAL WARD
BIO DATA 
 Name:Din Muhammad 
 Fa t h e r ’ s Name :Wazir Mu h ammad 
 65/M 
 Resident:Bara Dari , Lahore 
 Ocupation:Labourer 
 Marrital Status:Married 
 DOA:20/6/2014 
 MOD:Emergency 
 Registration No:966/14
PRESENTING COMPLAINS 
 A SOC ………1 d ay 
 Feve r……… 2 Day s
HISTORY OF PRESENTING ILLNESS 
My pt,a labourer by profession, hypertensive since 5 
years ,diabetic since 5 years, on oral 
hypoglycemics,was in his USOH when he developed 
ASOC since 1 day, sudden in onset, not associated 
with any fits,frothing,fecal or urinary incontinence, no 
c/o 
hemetemesis,melena,vomiting,diarrhea,anuria,decrea 
sed 
urination,bruising,bleeding(sepsis),nausea,vomiting,ab 
dominal pain or excessive urine production(dka),no 
h/o exposure to drugs or anesthetics(malignant 
hyperthermia),no c/o headache,neck rigidity or 
personality changes(encephalitis),no c/o weakness of 
any part of body, dif ficulty swallowing or vision trauma
HISTORY OF PRESENTING ILLNESS 
 ASOC was associated with fever since 1 day, sudden 
in onset, high grade,1 day 
duration,continuous,occuring throughout the day, not 
associated with any rigors or chills, no respiratory or 
urinary symptoms, with no night sweats, 
musculoskeletal pain, or neck rigidity.no relieving 
medicine used. There is no travel history, substance 
abuse, animal contact, sexual contact. His profession 
makes him exposed to bright sun daily. 
Contd….
SYSTEMIC REVIEW 
 RESPIRATORY SYSTEM…..No c/o cough, sputum 
 GIT…….No c/o vomiting,diarrhea,abdominal pain.no 
c/o altered bowel habits 
 CVS……Unremarkable
HISTORY 
PAST HISTORY: No such episode reported 
earlier, no previous hospital admissions 
Medical History:Pt taking oral hypoglycemics 
since 5 years. 
Surgical History: No operative history 
Family History: Siblings diabetic 
Personal History: Labourer by profession 
Socioeconomic status: Lower middle class
DIFFERENTIAL DIAGNOSIS 
HEAT STROKE 
Sepsis 
Diabetic ketoacidosis 
Malignant hyperthermia 
Encephalitis 
Cerebral malaria 
Cerebral hemorrhage
EXAMINATION 
 GENERAL PHYSICAL EXAMINATION(At presentation) 
 A 65 year old man, having normal physique, lying 
unconsciously on bed, with a branula on his right hand having 
vitals 
 BP….1 2 0 / 70 
 P u l s e….100 (puls e p r e s s ur e 5 0 , h i g h vo l ume ) 
 Temp……106 
 RR……. 24
GENERAL PHYSICAL EXAMINATION 
 Pal lor -ve 
 Cyanosis -ve 
 Clubbing -ve 
 Jaundice -ve 
 Leuconychia -ve 
 Koi lonychia -ve 
 Spl inter Haemorrhages Absent 
 Jane way lesions Absent 
 Os l e r ’ s n o d e s A b se n t 
 Palmar erythema Absent 
 Edema -ve 
 Lymph nodes -ve
CENTRAL NERVOUS SYSTEM 
AT PRESENTATION 
 Altered Sensorium, 
agitated 
 Pupils Reactive to light 
 Speech could not be 
assessed 
 Muscles have normal 
tone,bulk,power grade 
3/5(UL n LL) 
 Super ficial and deep 
tendon reflexes normal, 
Planters downgoing 
NOW 
Well groomed, alert 
 Pupils reactive to light 
 Speech normal 
 Muscles have normal 
tone,bulk,power grade 
5/5(UL n LL) 
 Super ficial and deep 
tendon reflexes normal, 
Planters downgoing
CENTRAL NERVOUS SYSTEM 
AT PRESENTATION 
 Coordination could not 
be assessed 
 Sensory Could not be 
assessed 
 Cranial Nerves(corneal 
and conjunctival 
reflexes present(5th 
cranial nerve)..gag and 
palatal reflexes 
intact(9th cranial nerve) 
NOW 
 Coordiantion normal 
 Sensory normal 
 Cranial nerves intact
CENTRAL NERVOUS SYSTEM 
 Glasgow Coma Scale. . At presentation 
EYE,2 MOTOR, 3 VERBAL,1 
Now 
EYE 4 MOTOR 6 VERBAL 5 
SOMI –ve 
No Focal Deficit
GENITOURINARY SYSTEM 
ABDOMEN 
 INSPECTION…neither sunken nor 
protuberant…no localized 
distension(hepatomegaly or 
splenomegaly)..abdomen moving 
correspondingly with respiration, no visible 
peristalsis 
Umbilicus…circular and inverted 
No scar marks, no visible pulsations, no 
striae,no prominent veins, with normal pubic 
hair distribution
GENITOURINARY SYSTEM 
PALPATION. On light palpation no 
localized or generalized rigidity or 
guarding. On deep palpation no 
rebound tenderness or mass. 
Liver, gall 
bladder,spleen,kidneys,urinary 
bladder, not palpable
GENITOURINARY SYSTEM 
PERCUSSION 
LIVER span 7cm 
Spleen and urinary bladder. 
Resonant percussion note 
Abdomen non distended…no free 
fluid, no fluid thrill or shifting 
dullness
GENITOURINARY SYSTEM 
Bowel sounds positive 
No bruit audible
CARDIOVASCULAR SYSTEM 
 INSPECTION…no chest deformity,bulging,scars 
pulsations or prominent veins 
 PALPATION…..apex beat at 5th ICS 1 cm 
medial to midclavicular line, no parasternal 
heave, heart sounds not palpable, no thrill 
 AUSCULTATION….1st heart sound audible at the 
apex with normal intensity and no splitting 
2nd heart sound audible at A1 area, normal 
intensity, no splitting
CARDIOVASCULAR SYSTEM 
No 3rd or 4th heart sounds 
No opening snap or ejection click, no 
sound of prosthetic valves, no 
murmurs or bruit
RESPIRATORY SYSTEM 
INSPECTION…RR 24…thoracoabdominal 
respiration, chest elliptical in shape, no 
prominent veins, pulsations or scar 
marks, chest moving equally bilaterally 
PALPATION…Trachea central in position, 
chest movement equal bilaterally, chest 
expansion 6cm,vocal fremitus normal on 
each side, no tenderness or crepitus
RESPIRATORY SYSTEM 
PERCUSSION…Resonant anteriorly 
and posteriorly 
AUSCULTATION….Normal vesicular 
breathing, no 
crepitations(tuberculosis),vocal 
resonance normal
HEAT STROKE 
MALIGNANT HYPERTHERMIA 
SEPSIS 
DIFFERENTIAL DIAGNOSIS
INVESTIGATIONS 
CBC 
 RBC ….4*106 /uL 
 HGB….13.1g/dL 
 HCT….57.1% 
MCV….91 .8 fL(80-100) 
MCH…..28pg(27-31) 
MCHC…..30.7g/dL(32-36) 
 PLT……20*106 /uL 
WBC…..12.2*103 /uL 
 NEU……78% 
 LYM……20% 
MO……4%
INVESTIGATIONS 
 Blood Urea…80.6 
 Creatinine….2.1 
 Na ….127 
 K….2.9 
 Bilirubin…0.7 
 ALT….127.8 
 AST….180.9 
 ALK Phosphate…..234 
 T.Protein…..6.6 
 Albumin…..3.6
INVESTIGATIONS 
PT….12/16 
APTT….32/38 
HbsAg….-ive 
AntiHCV….-ive
INVESTIGATIONS 
CK-NAC…..1270 
LDH…….994.6 
CK-MB…….43.5 
Ca….7.9 
Phosphorous……2.3
 pH….7.48 
 pCO2……26 
 HCO3…….19.3 
 Base excess….-4.1 
 Saturation…..95.7% 
 PO2…….71 
ABGS
INVESTIGATIONS 
URINE COMPLETE EXAMINATION 
Sp Gravity……1.000 
pH….6 
Protein….Nil 
Glucose….trace 
Ketones …Nil 
Bilirubin. Nil 
Pus cells…1-2
RADIOGRAPHY 
 USG ABDOMEN 
Normal scan 
Normal liver, spleen, pancreas, kidneys 
Normal urinary bladder, ureter, urethra, prostate 
ECG:rate 100,normal rhythem,normal axis with no 
ischemic changes 
CT scan…Dif fuse brain edema
FINAL DIAGNOSIS 
EXERTIONAL HEAT 
STROKE
HEAT STROKE 
 DEFINITION: It is a heat related illness characterized 
by elevated core body temperature (> 106 degree 
Fahrenheit) and dysfunction of CNS which results in 
confusion, delirium and coma. 
OR 
 heatstroke is a form of hyperthermia associated 
with the acute physiological alterations, the 
cytotoxicity of heat, systemic inflammatory response, 
oxidative damage and attenuated heat-shock 
response leading to a syndrome of multi-organ 
dysfunction.
HEAT RELATED ILLNESSES 
• Heat cramps: 
Heat cramps are caused by initial exposure to high 
temperatures or physical exer tion. 
• Heat exhaustion: 
Heat exhaustion occurs when you don't act on the 
signs and symptoms of heat cramps and your 
condition worsens. Signs and symptoms of heat 
exhaustion include a headache, dizziness or 
lightheadedness, nausea, skin that feels cool and 
moist, and muscle cramps. 
• Heat stroke
TYPES OF HEAT STROKE 
 CLASSIC NON EXHERTIONAL HEAT STROKE: 
Classic nonexer tional heatstroke (NEHS)is the one 
which occurs without involvement in any sor t of 
strenuous physical activity; more commonly af fects 
sedentary elderly individuals, persons who are 
chronically ill, and very young persons. 
 EXERTIONAL HEAT STROKE: 
Exer tional heatstroke (EHS) generally occurs in 
young individuals who engage in strenuous physical 
activity for a prolonged period of time in a hot 
environment.
SYMPTOMS 
High body temperature. 
A lack of sweating. 
Nausea and vomiting. 
Flushed skin. 
Rapid shallow breathing. 
Racing heart rate. 
Headache. 
Confusion. 
Unconsciousness. 
Muscle cramps or weakness.
RISK FACTORS 
 Young or old age: 
Both age groups usually have dif ficulty remaining 
hydrated, which also increases the risk. 
 Genetic response to heat stress: 
genetics may play a vital role in determining how 
body will respond in extremely hot conditions. 
 Sudden exposure to hot weather: 
No previous exposure to heat or humidity may 
increase the susceptible to heat -related illness on 
sudden exposure to high temperature. . 
.
CONTINUED 
 Certain medications. 
Some medications place you at a greater risk of 
heatstroke and other heat -related conditions 
because they af fect body's ability to stay hydrated 
and respond to heat . Beta blockers, diuretics, 
antidepressants or antipsychotics. Stimulants for 
attention-deficit/hyperactivity disorder (ADHD) and 
illegal stimulants such as amphetamines and 
cocaine 
 Thyrotoxicosis,tremors,sepsis 
may also increase the risk.
PRESENTATION ACCORDING TO AGE GROUP. 
9% 
37% 
17% 
37% 
1-25 YEARS 
25-50 YEARS 
50-75 YEARS 
>75 YEARS
MORTALITY ACCORDING TO AGE GROUP. 
1-25 years……10% 
25-50 years……30% 
50-70years…..40% 
>75 years,,,,,20%
1 to 25 
25 to 50 
50 to 75 
>75 
MORTALITY
HOW TO INVESTIGATE HEAT STROKE 
 ABGS…Respirator y alkalosis due to CNS stimulation 
...Metabolic acidosis due to Lactic Acidosis 
Electrolytes. Hypernatremia...water loss, dehydration 
Hyponatremia… hypotonic solutions, 
free water, diuretics, excessive sweat sodium 
losses. 
Potassium: Hypokalemia 
Other: Hypophosphatemia…… phosphaturia 
Hyperphosphatemia…….rhabdomyolysis , 
Hypocalcemia ++ calcium binding in damaged 
muscle, Hypomagnesaemia .
 Hepatic Injury 
 ^^ALT,AST 
INVESTIGATIONS 
Muscle function tests 
 Creatinine kinase (CK), lactate dehydrogenase (LDH), 
aldolase, and myoglobin commonly are released 
from muscles when muscle necrosis occurs. 
 CK levels exceeding 100,000 IU/mL are common in 
patients with EHS. 
 Elevations in myoglobin may not be noted despite 
muscle necrosis because myoglobin is metabolized 
rapidly by the liver and excreted rapidly by the 
kidneys.
COMPLETE BLOOD CELL COUNT 
 ^^ WBC count 
 Low plt count 
 RFT 
^ serum uric acid 
creatinine 
BUN 
URINE C/E 
RBCS 
Proteinuria 
 CSF 
 ^protein ..150mg/dL
IMAGING STUDIES 
CT SCAN…to rule out CNS injury
ELECTROCARDIOGRAPHY 
: Sinus tachycardia of 130-140 beats per 
minute and nonspecific and ischemic ST-T 
wave abnormalities are common. In 
addition, a number of conduction 
abnormalities (eg, right bundle branch 
block), prolonged QT interval) may be 
noted.
COMPLICATIONS 
 CNS…..CEREBRAL EDEMA,HERNIATION,COMA 
 CVS…HIGH OUTPUT CARDIAC FAILURE<LOW 
OUTPUT CARDIAC FAILURE 
 HEPATIC…….HEPATIC INJURY,FULMINANT 
HEPATIC FAILURE,DIC 
MUSCULOSKELETAL…..RHABDOMYOLYSIS 
 RENAL…….ACUTE KIDNEY INJURY 
 RESPIRATORY…….PULMONARY 
INFARCTION,ASPIRATION 
PNEUMONIA,PULMONARY EDEMA
TREATMENT 
Rapid reduction of core body temperature 
patients diagnosed with exertional heatstroke 
(EHS) or nonexertional heatstroke (NEHS) 
should be admitted to the hospital for at least 
48 hours to monitor for complications. 
cooling must begin immediately and must be 
continued during the patient's resuscitation
TREATMENT 
 The basic premise of rapidly lowering the core 
temperature to about 39°C (to avoid overshooting 
and rebound hyper thermia) remains the primary 
goal. 
 Rectal temperature should be obtained instead of 
oral temperature 
 Lower core body temperature to 390 C (0.20 
C/min),halt at 390 C to prevent iatrogenic 
hypothermia 
 Removal of restrictive clothing and spraying water on 
the body, covering the patient with ice water–soaked 
sheets, or placing ice packs in the axillae and groin 
may reduce the patient's temperature significantly
TREATMENT 
Patients who are unable to protect their 
airway should be intubated. Patients who 
are awake and responsive should receive 
supplemental oxygen.
 IV Lines 
TREATMENT 
Dextrose Water(50%)
 Thermometer 
 NG Tube 
 Foleys catheter 
TREATMENT
ICE WATER IMMERSION 
 Advantages: Rapidly lowers core body temperature in 
20-40 mins 
 Disadvantages: 
Uncomfortable, subcutaneous vasoconstriction, 
shivering
EVAPORATIVE HEAT LOSS 
Removal of pts. clothes 
Intermittent spay of warm 
water 
Power ful fan blow
OTHER TECQNIQUES 
Peritoneal Lavage 
Thoracic Lavage 
Rectal Lavage 
Gastric lavage 
Cold IV fluids 
Cold humidified oxygen
OTHER COOLING TECHNIQUES 
Cold IV fluids 
Cold humidified oxygen 
Cooling blankets 
Wet towels
BENZODIAZEPINES/BARBITURATES 
In patients with Shivering and 
agitation….to stop excessive heat 
production 
In patients developing convulsions 
Mechanical ventilation(refractory 
convulsions) 
EEG Monitoring
ANTIPYRETICS 
Aggravate bleeding tendency in patients who 
have developed hepatic, renal or hematologic 
complications 
ANTIPYRETICS
NEUROLEPTICS 
 Lower seizure threshold 
 Inter fere with thermoregulation 
 Anticholinergic 
 Hypotension 
 Hepatotoxic
FLUID RESUSCITATION 
Volume depletion determined by 
 pulse,Bp,Urine output 
CVP line
DOBUTAMINE 
Less arrythmogenic
ALPHA ADRENERGIC DRUGS 
 vasoconstriction 
 Inter fere with heat loss
RHABDOMAYOLYSIS 
 Dark tea-coloured urine tender edematous 
muscles 
Myoglobin Acute kidney injury
RHABDOMYOLYSIS TREATMENT 
Treatment 
IV Fluids(10 L) 
Urine Alkalinization to pH of 7.5-8(prevents 
myoglobin precipitation, controls acidosis, 
hyperkalemia) 
Mannitol(^ renal blood flow, urine output, free 
radical scavenger) 
Urine Output 3ml/kg/h 
 Renal Failure………>Dialysis
METABOLIC SUPPORT 
 Hyperkalemia 
 Hypocalcaemia ARRHYTHMIAS 
 Hyperphosphatemia 
 Hyperkalemia…..Hyper tonic dextrose 
NaHCO3 
Insulin( in liver failure who 
develop hypoglycemia) 
 Ca corrected if pt has ventricular 
ectopy,convulsions,hyperkalemia
HEPATIC INJURY 
Elevations in transaminase levels and 
bilirubin. 
Hypoglycemia, 
 Abnormal coagulation 
 
Dextrose Solutions 
Replacement of 
clotting factors, fresh frozen plasma, platelets, 
and blood
PULMONARY INJURY 
Pulmonary edema 
due to 
aggressive 
rehydration, renal failure, congestive heart 
failure, and ARDS. 
ARDS treatment mechanical 
ventilation 
positive end-expiratory pressure (PEEP).
RENAL INJURY 
Direct thermal injury 
Myoglobinuria, 
Hypotension, 
Acute tubular necrosis 
Treatment 
Intravenous fluids, 
Diuretics 
correction of associated acid-base and electrolyte 
abnormalities
THANK YOU

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Heat stroke by dr nida

  • 1. CASE PRESENTATION NIDA EILY PGR WEST MEDICAL WARD
  • 2. BIO DATA  Name:Din Muhammad  Fa t h e r ’ s Name :Wazir Mu h ammad  65/M  Resident:Bara Dari , Lahore  Ocupation:Labourer  Marrital Status:Married  DOA:20/6/2014  MOD:Emergency  Registration No:966/14
  • 3. PRESENTING COMPLAINS  A SOC ………1 d ay  Feve r……… 2 Day s
  • 4. HISTORY OF PRESENTING ILLNESS My pt,a labourer by profession, hypertensive since 5 years ,diabetic since 5 years, on oral hypoglycemics,was in his USOH when he developed ASOC since 1 day, sudden in onset, not associated with any fits,frothing,fecal or urinary incontinence, no c/o hemetemesis,melena,vomiting,diarrhea,anuria,decrea sed urination,bruising,bleeding(sepsis),nausea,vomiting,ab dominal pain or excessive urine production(dka),no h/o exposure to drugs or anesthetics(malignant hyperthermia),no c/o headache,neck rigidity or personality changes(encephalitis),no c/o weakness of any part of body, dif ficulty swallowing or vision trauma
  • 5. HISTORY OF PRESENTING ILLNESS  ASOC was associated with fever since 1 day, sudden in onset, high grade,1 day duration,continuous,occuring throughout the day, not associated with any rigors or chills, no respiratory or urinary symptoms, with no night sweats, musculoskeletal pain, or neck rigidity.no relieving medicine used. There is no travel history, substance abuse, animal contact, sexual contact. His profession makes him exposed to bright sun daily. Contd….
  • 6. SYSTEMIC REVIEW  RESPIRATORY SYSTEM…..No c/o cough, sputum  GIT…….No c/o vomiting,diarrhea,abdominal pain.no c/o altered bowel habits  CVS……Unremarkable
  • 7. HISTORY PAST HISTORY: No such episode reported earlier, no previous hospital admissions Medical History:Pt taking oral hypoglycemics since 5 years. Surgical History: No operative history Family History: Siblings diabetic Personal History: Labourer by profession Socioeconomic status: Lower middle class
  • 8. DIFFERENTIAL DIAGNOSIS HEAT STROKE Sepsis Diabetic ketoacidosis Malignant hyperthermia Encephalitis Cerebral malaria Cerebral hemorrhage
  • 9. EXAMINATION  GENERAL PHYSICAL EXAMINATION(At presentation)  A 65 year old man, having normal physique, lying unconsciously on bed, with a branula on his right hand having vitals  BP….1 2 0 / 70  P u l s e….100 (puls e p r e s s ur e 5 0 , h i g h vo l ume )  Temp……106  RR……. 24
  • 10. GENERAL PHYSICAL EXAMINATION  Pal lor -ve  Cyanosis -ve  Clubbing -ve  Jaundice -ve  Leuconychia -ve  Koi lonychia -ve  Spl inter Haemorrhages Absent  Jane way lesions Absent  Os l e r ’ s n o d e s A b se n t  Palmar erythema Absent  Edema -ve  Lymph nodes -ve
  • 11. CENTRAL NERVOUS SYSTEM AT PRESENTATION  Altered Sensorium, agitated  Pupils Reactive to light  Speech could not be assessed  Muscles have normal tone,bulk,power grade 3/5(UL n LL)  Super ficial and deep tendon reflexes normal, Planters downgoing NOW Well groomed, alert  Pupils reactive to light  Speech normal  Muscles have normal tone,bulk,power grade 5/5(UL n LL)  Super ficial and deep tendon reflexes normal, Planters downgoing
  • 12. CENTRAL NERVOUS SYSTEM AT PRESENTATION  Coordination could not be assessed  Sensory Could not be assessed  Cranial Nerves(corneal and conjunctival reflexes present(5th cranial nerve)..gag and palatal reflexes intact(9th cranial nerve) NOW  Coordiantion normal  Sensory normal  Cranial nerves intact
  • 13. CENTRAL NERVOUS SYSTEM  Glasgow Coma Scale. . At presentation EYE,2 MOTOR, 3 VERBAL,1 Now EYE 4 MOTOR 6 VERBAL 5 SOMI –ve No Focal Deficit
  • 14. GENITOURINARY SYSTEM ABDOMEN  INSPECTION…neither sunken nor protuberant…no localized distension(hepatomegaly or splenomegaly)..abdomen moving correspondingly with respiration, no visible peristalsis Umbilicus…circular and inverted No scar marks, no visible pulsations, no striae,no prominent veins, with normal pubic hair distribution
  • 15. GENITOURINARY SYSTEM PALPATION. On light palpation no localized or generalized rigidity or guarding. On deep palpation no rebound tenderness or mass. Liver, gall bladder,spleen,kidneys,urinary bladder, not palpable
  • 16. GENITOURINARY SYSTEM PERCUSSION LIVER span 7cm Spleen and urinary bladder. Resonant percussion note Abdomen non distended…no free fluid, no fluid thrill or shifting dullness
  • 17. GENITOURINARY SYSTEM Bowel sounds positive No bruit audible
  • 18. CARDIOVASCULAR SYSTEM  INSPECTION…no chest deformity,bulging,scars pulsations or prominent veins  PALPATION…..apex beat at 5th ICS 1 cm medial to midclavicular line, no parasternal heave, heart sounds not palpable, no thrill  AUSCULTATION….1st heart sound audible at the apex with normal intensity and no splitting 2nd heart sound audible at A1 area, normal intensity, no splitting
  • 19. CARDIOVASCULAR SYSTEM No 3rd or 4th heart sounds No opening snap or ejection click, no sound of prosthetic valves, no murmurs or bruit
  • 20. RESPIRATORY SYSTEM INSPECTION…RR 24…thoracoabdominal respiration, chest elliptical in shape, no prominent veins, pulsations or scar marks, chest moving equally bilaterally PALPATION…Trachea central in position, chest movement equal bilaterally, chest expansion 6cm,vocal fremitus normal on each side, no tenderness or crepitus
  • 21. RESPIRATORY SYSTEM PERCUSSION…Resonant anteriorly and posteriorly AUSCULTATION….Normal vesicular breathing, no crepitations(tuberculosis),vocal resonance normal
  • 22. HEAT STROKE MALIGNANT HYPERTHERMIA SEPSIS DIFFERENTIAL DIAGNOSIS
  • 23. INVESTIGATIONS CBC  RBC ….4*106 /uL  HGB….13.1g/dL  HCT….57.1% MCV….91 .8 fL(80-100) MCH…..28pg(27-31) MCHC…..30.7g/dL(32-36)  PLT……20*106 /uL WBC…..12.2*103 /uL  NEU……78%  LYM……20% MO……4%
  • 24. INVESTIGATIONS  Blood Urea…80.6  Creatinine….2.1  Na ….127  K….2.9  Bilirubin…0.7  ALT….127.8  AST….180.9  ALK Phosphate…..234  T.Protein…..6.6  Albumin…..3.6
  • 25. INVESTIGATIONS PT….12/16 APTT….32/38 HbsAg….-ive AntiHCV….-ive
  • 26. INVESTIGATIONS CK-NAC…..1270 LDH…….994.6 CK-MB…….43.5 Ca….7.9 Phosphorous……2.3
  • 27.  pH….7.48  pCO2……26  HCO3…….19.3  Base excess….-4.1  Saturation…..95.7%  PO2…….71 ABGS
  • 28. INVESTIGATIONS URINE COMPLETE EXAMINATION Sp Gravity……1.000 pH….6 Protein….Nil Glucose….trace Ketones …Nil Bilirubin. Nil Pus cells…1-2
  • 29. RADIOGRAPHY  USG ABDOMEN Normal scan Normal liver, spleen, pancreas, kidneys Normal urinary bladder, ureter, urethra, prostate ECG:rate 100,normal rhythem,normal axis with no ischemic changes CT scan…Dif fuse brain edema
  • 31. HEAT STROKE  DEFINITION: It is a heat related illness characterized by elevated core body temperature (> 106 degree Fahrenheit) and dysfunction of CNS which results in confusion, delirium and coma. OR  heatstroke is a form of hyperthermia associated with the acute physiological alterations, the cytotoxicity of heat, systemic inflammatory response, oxidative damage and attenuated heat-shock response leading to a syndrome of multi-organ dysfunction.
  • 32. HEAT RELATED ILLNESSES • Heat cramps: Heat cramps are caused by initial exposure to high temperatures or physical exer tion. • Heat exhaustion: Heat exhaustion occurs when you don't act on the signs and symptoms of heat cramps and your condition worsens. Signs and symptoms of heat exhaustion include a headache, dizziness or lightheadedness, nausea, skin that feels cool and moist, and muscle cramps. • Heat stroke
  • 33. TYPES OF HEAT STROKE  CLASSIC NON EXHERTIONAL HEAT STROKE: Classic nonexer tional heatstroke (NEHS)is the one which occurs without involvement in any sor t of strenuous physical activity; more commonly af fects sedentary elderly individuals, persons who are chronically ill, and very young persons.  EXERTIONAL HEAT STROKE: Exer tional heatstroke (EHS) generally occurs in young individuals who engage in strenuous physical activity for a prolonged period of time in a hot environment.
  • 34. SYMPTOMS High body temperature. A lack of sweating. Nausea and vomiting. Flushed skin. Rapid shallow breathing. Racing heart rate. Headache. Confusion. Unconsciousness. Muscle cramps or weakness.
  • 35. RISK FACTORS  Young or old age: Both age groups usually have dif ficulty remaining hydrated, which also increases the risk.  Genetic response to heat stress: genetics may play a vital role in determining how body will respond in extremely hot conditions.  Sudden exposure to hot weather: No previous exposure to heat or humidity may increase the susceptible to heat -related illness on sudden exposure to high temperature. . .
  • 36. CONTINUED  Certain medications. Some medications place you at a greater risk of heatstroke and other heat -related conditions because they af fect body's ability to stay hydrated and respond to heat . Beta blockers, diuretics, antidepressants or antipsychotics. Stimulants for attention-deficit/hyperactivity disorder (ADHD) and illegal stimulants such as amphetamines and cocaine  Thyrotoxicosis,tremors,sepsis may also increase the risk.
  • 37. PRESENTATION ACCORDING TO AGE GROUP. 9% 37% 17% 37% 1-25 YEARS 25-50 YEARS 50-75 YEARS >75 YEARS
  • 38. MORTALITY ACCORDING TO AGE GROUP. 1-25 years……10% 25-50 years……30% 50-70years…..40% >75 years,,,,,20%
  • 39. 1 to 25 25 to 50 50 to 75 >75 MORTALITY
  • 40. HOW TO INVESTIGATE HEAT STROKE  ABGS…Respirator y alkalosis due to CNS stimulation ...Metabolic acidosis due to Lactic Acidosis Electrolytes. Hypernatremia...water loss, dehydration Hyponatremia… hypotonic solutions, free water, diuretics, excessive sweat sodium losses. Potassium: Hypokalemia Other: Hypophosphatemia…… phosphaturia Hyperphosphatemia…….rhabdomyolysis , Hypocalcemia ++ calcium binding in damaged muscle, Hypomagnesaemia .
  • 41.  Hepatic Injury  ^^ALT,AST INVESTIGATIONS Muscle function tests  Creatinine kinase (CK), lactate dehydrogenase (LDH), aldolase, and myoglobin commonly are released from muscles when muscle necrosis occurs.  CK levels exceeding 100,000 IU/mL are common in patients with EHS.  Elevations in myoglobin may not be noted despite muscle necrosis because myoglobin is metabolized rapidly by the liver and excreted rapidly by the kidneys.
  • 42. COMPLETE BLOOD CELL COUNT  ^^ WBC count  Low plt count  RFT ^ serum uric acid creatinine BUN URINE C/E RBCS Proteinuria  CSF  ^protein ..150mg/dL
  • 43. IMAGING STUDIES CT SCAN…to rule out CNS injury
  • 44. ELECTROCARDIOGRAPHY : Sinus tachycardia of 130-140 beats per minute and nonspecific and ischemic ST-T wave abnormalities are common. In addition, a number of conduction abnormalities (eg, right bundle branch block), prolonged QT interval) may be noted.
  • 45. COMPLICATIONS  CNS…..CEREBRAL EDEMA,HERNIATION,COMA  CVS…HIGH OUTPUT CARDIAC FAILURE<LOW OUTPUT CARDIAC FAILURE  HEPATIC…….HEPATIC INJURY,FULMINANT HEPATIC FAILURE,DIC MUSCULOSKELETAL…..RHABDOMYOLYSIS  RENAL…….ACUTE KIDNEY INJURY  RESPIRATORY…….PULMONARY INFARCTION,ASPIRATION PNEUMONIA,PULMONARY EDEMA
  • 46. TREATMENT Rapid reduction of core body temperature patients diagnosed with exertional heatstroke (EHS) or nonexertional heatstroke (NEHS) should be admitted to the hospital for at least 48 hours to monitor for complications. cooling must begin immediately and must be continued during the patient's resuscitation
  • 47. TREATMENT  The basic premise of rapidly lowering the core temperature to about 39°C (to avoid overshooting and rebound hyper thermia) remains the primary goal.  Rectal temperature should be obtained instead of oral temperature  Lower core body temperature to 390 C (0.20 C/min),halt at 390 C to prevent iatrogenic hypothermia  Removal of restrictive clothing and spraying water on the body, covering the patient with ice water–soaked sheets, or placing ice packs in the axillae and groin may reduce the patient's temperature significantly
  • 48. TREATMENT Patients who are unable to protect their airway should be intubated. Patients who are awake and responsive should receive supplemental oxygen.
  • 49.  IV Lines TREATMENT Dextrose Water(50%)
  • 50.  Thermometer  NG Tube  Foleys catheter TREATMENT
  • 51. ICE WATER IMMERSION  Advantages: Rapidly lowers core body temperature in 20-40 mins  Disadvantages: Uncomfortable, subcutaneous vasoconstriction, shivering
  • 52. EVAPORATIVE HEAT LOSS Removal of pts. clothes Intermittent spay of warm water Power ful fan blow
  • 53. OTHER TECQNIQUES Peritoneal Lavage Thoracic Lavage Rectal Lavage Gastric lavage Cold IV fluids Cold humidified oxygen
  • 54. OTHER COOLING TECHNIQUES Cold IV fluids Cold humidified oxygen Cooling blankets Wet towels
  • 55. BENZODIAZEPINES/BARBITURATES In patients with Shivering and agitation….to stop excessive heat production In patients developing convulsions Mechanical ventilation(refractory convulsions) EEG Monitoring
  • 56. ANTIPYRETICS Aggravate bleeding tendency in patients who have developed hepatic, renal or hematologic complications ANTIPYRETICS
  • 57. NEUROLEPTICS  Lower seizure threshold  Inter fere with thermoregulation  Anticholinergic  Hypotension  Hepatotoxic
  • 58. FLUID RESUSCITATION Volume depletion determined by  pulse,Bp,Urine output CVP line
  • 60. ALPHA ADRENERGIC DRUGS  vasoconstriction  Inter fere with heat loss
  • 61. RHABDOMAYOLYSIS  Dark tea-coloured urine tender edematous muscles Myoglobin Acute kidney injury
  • 62. RHABDOMYOLYSIS TREATMENT Treatment IV Fluids(10 L) Urine Alkalinization to pH of 7.5-8(prevents myoglobin precipitation, controls acidosis, hyperkalemia) Mannitol(^ renal blood flow, urine output, free radical scavenger) Urine Output 3ml/kg/h  Renal Failure………>Dialysis
  • 63. METABOLIC SUPPORT  Hyperkalemia  Hypocalcaemia ARRHYTHMIAS  Hyperphosphatemia  Hyperkalemia…..Hyper tonic dextrose NaHCO3 Insulin( in liver failure who develop hypoglycemia)  Ca corrected if pt has ventricular ectopy,convulsions,hyperkalemia
  • 64. HEPATIC INJURY Elevations in transaminase levels and bilirubin. Hypoglycemia,  Abnormal coagulation  Dextrose Solutions Replacement of clotting factors, fresh frozen plasma, platelets, and blood
  • 65. PULMONARY INJURY Pulmonary edema due to aggressive rehydration, renal failure, congestive heart failure, and ARDS. ARDS treatment mechanical ventilation positive end-expiratory pressure (PEEP).
  • 66. RENAL INJURY Direct thermal injury Myoglobinuria, Hypotension, Acute tubular necrosis Treatment Intravenous fluids, Diuretics correction of associated acid-base and electrolyte abnormalities