Heat stroke by dr nida

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


Glasgow Coma Scale.. At presentation

EYE,2 MOTOR, 3 VERBAL,1

Now

EYE 4 MOTOR 6 VERBAL 5

SOMI –ve

No Focal Deficit


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


PERCUSSION

LIVER span 7cm

Spleen and urinary bladder.

Resonant percussion note

Abdomen non distended…no free

fluid, no fluid thrill or shifting

dullness


Bowel sounds positive

No bruit audible


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

Heat stroke by dr nida

Health & Medicine

Transcript of Heat stroke by dr nida