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
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….
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
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
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
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.
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.
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.
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.
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
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