heat stroke by dr nida
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CASE PRESENTATION
NIDA EILY
PGR WEST MEDICAL WARD
Name:Din Muhammad
Father’s Name:Wazir Muhammad
65/M
Resident:Bara Dari, Lahore
Ocupation:Labourer
Marrital Status:Married
DOA:20/6/2014
MOD:Emergency
Registration No:966/14
BIO DATA
ASOC ………1 day
Fever……… 2 Days
PRESENTING COMPLAINS
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, difficulty 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….
HISTORY OF PRESENTING ILLNESS
RESPIRATORY SYSTEM…..No c/o cough, sputum
GIT…….No c/o vomiting,diarrhea,abdominal pain.no
c/o altered bowel habits
CVS……Unremarkable
SYSTEMIC REVIEW
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
HISTORY
HEAT STROKE
Sepsis
Diabetic ketoacidosis
Malignant hyperthermia
Encephalitis
Cerebral malaria
Cerebral hemorrhage
DIFFERENTIAL DIAGNOSIS
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….120/70
Pulse….100(pulse pressure 50,high volume)
Temp……106
RR…….24
EXAMINATION
Pallor -ve
Cyanosis -ve
Clubbing -ve
Jaundice -ve
Leuconychia -ve
Koilonychia -ve
Splinter Haemorrhages Absent
Jane way lesions Absent
Osler’s nodes Absent
Palmar erythema Absent
Edema -ve
Lymph nodes -ve
GENERAL PHYSICAL EXAMINATION
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)
Superficial 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)
Superficial 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(5 th
cranial nerve)..gag and palatal reflexes intact(9 th 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
CENTRAL NERVOUS SYSTEM
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
ABDOMEN
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
GENITOURINARY 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
CARDIOVASCULAR 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
RESPIRATORY SYSTEM
HEAT STROKE
MALIGNANT HYPERTHERMIA
SEPSIS
DIFFERENTIAL DIAGNOSIS
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
INVESTIGATIONS
pH….7.48
pCO2……26
HCO3…….19.3
Base excess….-4.1
Saturation…..95.7%
PO2…….71
ABGS
URINE COMPLETE EXAMINATION
Sp Gravity……1.000
pH….6
Protein….Nil
Glucose….trace
Ketones …Nil
Bilirubin. Nil
Pus cells…1-2
INVESTIGATIONS
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…Diffuse brain edema
RADIOGRAPHY
EXERTIONAL HEAT
STROKE
FINAL DIAGNOSIS
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 exertion.
• 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 nonexertional heatstroke (NEHS)is the one
which occurs without involvement in any sort of
strenuous physical activity; more commonly affects
sedentary elderly individuals, persons who are
chronically ill, and very young persons.
EXERTIONAL HEAT STROKE:
Exertional 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 difficulty 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 affect 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%37%
17%
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
ABGS…Respiratory 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 .
HOW TO INVESTIGATE HEAT STROKE
Hepatic Injury
^^ALT,AST
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.
INVESTIGATIONS
^^ WBC count
Low plt count
RFT
^ serum uric acid
creatinine
BUN
URINE C/E
RBCS
Proteinuria
CSF
^protein ..150mg/dL
COMPLETE BLOOD CELL COUNT
CT SCAN…to rule out CNS injury
IMAGING STUDIES
: 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 .
ELECTROCARDIOGRAPHY
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
COMPLICATIONS
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 hyperthermia) 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.
TREATMENT
IV Lines
Dextrose Water(50%)
TREATMENT
Thermometer
NG Tube
Foleys catheter
TREATMENT
Advantages: Rapidly lowers core body temperature in
20-40 mins
Disadvantages:
Uncomfortable, subcutaneous vasoconstriction,
shivering
ICE WATER IMMERSION
Removal of pts. clothes
Intermittent spay of warm
water
Powerful fan blow
EVAPORATIVE HEAT LOSS
Peritoneal Lavage
Thoracic Lavage
Rectal Lavage
Gastric lavage
Cold IV fluids
Cold humidified oxygen
OTHER TECQNIQUES
Cold IV fluids
Cold humidified oxygen
Cooling blankets
Wet towels
OTHER COOLING TECHNIQUES
In patients with Shivering and
agitation….to stop excessive heat
production
In patients developing convulsions
Mechanical ventilation(refractory
convulsions)
EEG Monitoring
BENZODIAZEPINES/BARBITURATES
Aggravate bleeding tendency in patients who
have developed hepatic, renal or hematologic
complications
ANTIPYRETICS
ANTIPYRETICS
Lower seizure threshold
Interfere with thermoregulation
Anticholinergic
Hypotension
Hepatotoxic
NEUROLEPTICS
Volume depletion determined by
pulse,Bp,Urine output
CVP line
FLUID RESUSCITATION
Less arrythmogenic
DOBUTAMINE
vasoconstriction
Interfere with heat loss
ALPHA ADRENERGIC DRUGS
Dark tea-coloured urine tender edematous
muscles
Myoglobin Acute kidney injury
RHABDOMAYOLYSIS
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
RHABDOMYOLYSIS TREATMENT
Hyperkalemia
Hypocalcaemia ARRHYTHMIAS
Hyperphosphatemia
Hyperkalemia…..Hypertonic dextrose
NaHCO3
Insulin( in liver failure who
develop hypoglycemia)
Ca corrected if pt has ventricular
ectopy,convulsions,hyperkalemia
METABOLIC SUPPORT
Elevations in transaminase levels and
bilirubin.
Hypoglycemia,
Abnormal coagulation
Dextrose Solutions
Replacement of
clotting factors, fresh frozen plasma, platelets,
and blood
HEPATIC INJURY
Pulmonary edema
due to
aggressive
rehydration, renal failure, congestive heart
failure, and ARDS.
ARDS treatment mechanical
ventilation
positive end-expiratory pressure (PEEP).
PULMONARY INJURY
Direct thermal injury
Myoglobinuria,
Hypotension,
Acute tubular necrosis
Treatment
Intravenous fluids,
Diuretics
correction of associated acid-base and electrolyte
abnormalities
RENAL INJURY
THANK YOU
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