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CHAPTER II

DISCUSSION

2.1 Tutorial Data


Tutor : dr. R.A. Tanzila, M.Kes
Moderator : Muhammad Dzaky Jalaluddin
Desk Secretary : Olive Mutiara Alzena
Board Secretary : Ghea Lingga Septiareni
Date and Time :
1. Tuesday, July 17th 2017
Time: 08.00 – 10.30 WIB
2. Thursday, July 18th 2017
Time: 08.00 – 10.30 WIB
Rules :
1. All students must actively participate.
2. One must raise hand before giving arguments.
3. All students must speak with manners and respect
each other’s opinion.
4. One must ask for moderator or tutor permission
before leaving the room.
2.2 Case
"Help My Boy"

Yantok, a boy, 4 year old, BW 16 kg brought by his mother to ER RSMP at 2


pm, due to loss of consciousness since 1 hour. Two hours ago, Yantok was
suffered general convulsion during five minutes. At 9 am, Yantok brought by
his mother when queue “sembako” at Monpera. Yantok began sweating and
felt warm in whole body at 12 pm when the wheater was sweltering.
Physical Examination:
Primary Survey:
- Airway : No snoring.
- Breathing : RR 32x/minutes, no rales, no wheezing.
- Circulation: BP 90/70 mmHg, PR 140x/minutes, hot extremities, capillary
refilled time < 3 second.
- Disability : Eyes opening response to pain, best motor response move to
localized pain, best verbal response, inappropriate words, normal pupil,
sight reflex (+).
- Exposure :
Temperature 41oC
General flushing
Secondary Survey:
- Head :
Eye : Normal conjungtiva.
Nose : Breath of the nostrils (-).
Ear : No abnormality.
Mouth: Dry lips.
- Neck : In normal limit.
- Chest : In normal limit.
- Abdomen : In normal limit.
- Upper and lower extremities: Hot and flushing.
2.3 Clarification of Terms
Tabel 2.1. Terms List
Terms Explanation
Consciousness Is the state of quality awareness.
General flushing Reddening on the whole body results
from dilatation of the blood vessel
beneath the skin surface which can be
caused by high temperature.
Sight reflex Refex of pupil that react from the
light to control the intensity of light.
Rales An abnormal crackling or rattling
sound heard upon auscultation of the
chest.
Capillary refilled time Time taken for color to return an
external capillary bed after pressure
his applied to cause blanching.
The nostril breathing Breathing with additional help of the
nose movement.
Wheezing Rattling sound in the chest as the
result of obstruction in the air
passage.
Convulsion Involunteer contraction of muscle.

2.4 Problem Identification


1. Yantok, a boy, 4 year old, BW 16 kg brought by his mother to ER RSMP
at 2 pm, due to loss of consciousness since 1 hour.
2. Two hours ago, Yantok was suffered general convulsion during five
minutes. At 9 am, Yantok brought by his mother when queue “sembako”
at Monpera. Yantok began sweating and felt warm in whole body at 12
pm when the wheater was sweltering.
3. Physical Examination: Primary Survey.
4. Physical Examination: Secondary Survey.
1.2 Problem Analysis
1. Yantok, a boy, 4 year old, BW 16 kg brought by his mother to ER RSMP
at 2 pm, due to loss of consciousness since 1 hour.
a. What is the etiology of losing consciousness?
Answer:
According to Tyagi et al in 2009, syncope caused by conditions that
do not directly involve the heart includes:
a. A shift in body position from lying or sitting to a more vertical
position
b. Dehydration
c. Blood pressure medications
d. Parkinson’s disease
e. Diseases of the nervesto the legs of the elderly
Synthesis:
According to Khan et al in 2015, there can be different underlying
causes of syncope, which are:
a. Neurocardiogenic syncope
Results when something triggers a short-term malfunction of the
autonomous nervous system (ANS). It is also known as neurally
mediated syncope (NMS).The ANS affects heart rate, digestion,
respiration rate, salivation, perspiration, diameter of the pupils,
urination, and sexual arousal. Most of these actions are
involuntary, but some, such as breathing, can also be done
consciously.There will be a drop in blood pressure and the
heartbeat and pulse rate will slow down. This causes a
temporary interruption in the brain's blood and oxygen supply.
Possible triggers include:
a. suddenly seeing something that is unpleasant or shocking,
such as blood
b. sudden exposure to an unpleasant sight or experience
c. sudden emotional upset, for example when receiving bad
news
d. extreme embarrassment
e. standing still for a long time
f. being in a hot and stuffy place for a long time
b. Occupational or situational syncope
Is a type of Neurocardiogenic syncope, but the link is physical
rather than emotional, mental, or abstract. Triggers may include:
a. coughing or sneezing
b. laughing or swallowing
c. defecating or urinating
d. demanding physical activities, such as lifting a heavy
weight
c. Orthostatic hypotension
Can happen when a person faints after stands up rapidly from a
seated or lying down position. Gravity pulls blood down to the
legs, resulting in lower blood pressure elsewhere. Normally, the
body's nervous system reacts by raising the heart beat and
narrowing blood vessels. This stabilizes blood pressure.
However, if something undermines this stabilization process,
there may be poor blood and oxygen supply to the brain, leading
to fainting. Triggers include:
a. Dehydration: If body fluid levels drop, so will blood
pressure. This can make it harder for the body to stabilize
blood pressure, resulting in less blood and oxygen reaching
the brain.
b. Untreated diabetes: A person with diabetes may urinate
more often, leading to dehydration. High blood glucose
levels can lead to damage in some nerves, especially those
that regulate blood pressure.
c. Some medications: Diuretics, beta-blockers and anti-
hypertensive drugs may cause orthostatic hypotension in
some people.
d. Alcohol: Some people faint if they consume too much
alcohol in a short space of time.
e. Some neurological conditions: Parkinson's disease and other
conditions affect the nervous systems, and this can lead to
orthostatic hypotension.
f. Carotid sinus syndrome: Pressure on the pressure sensors in
the carotid artery can cause fainting. These pressure sensors
are known as the carotid sinus. The carotid artery is the
main artery that supplies blood to the brain.
g. If the carotid sinus is over-sensitive, blood pressure may
drop if it is physically stimulated, resulting in fainting.
Examples include turning the head to one side, wearing a
tight collar or tie, or pressing over the carotid sinus while
shaving. This is more common among males aged over 50
years.
d. Cardiac syncope
An underlying heart problem can cause a drop in blood and
oxygen supply to the brain. Possible conditions include:
a. arrhythmias, or abnormal heart beat
b. stenosis, a blockage of the heart valves
c. hypertension, or high blood pressure
d. a heart attack, when a heart muscle dies because of a lack of
blood and oxygen
i. This cause of fainting will usually need treatment and
monitoring.
b. What is the classification of consciousness?
Answer:
Classification of consciousness can be divided into conscious,
confuse, asleep, stupor, and coma.
Synthesis:
According to Woerlee in 2015, there are five classifications of
consciousness, which are:
1. Conscious, is the patient normally conscious and oriented, as well
as having normal spontaneous speech, intellectual activity and
movement.
2. Drowsy or confused, the patient is inattentive, may not manifest
any spontaneous activity or speech. When stimulated he will react
appropriately both with speech and movement. May be
disoriented but can carry outsimple commands.
3. Asleep, the patient is asleep unless stimulated, being accessible to
verbal stimulation or touch, but when awake is usually
disoriented.
4. Stupor, the patient is not conscious unless stimulated. Manifasts
no spontaneous behavior, except for twitching, or other automatic
abnormal movements. Responds only minimally to shouting or
light pain stimuli.
5. Coma, the patient is unconscious. Only reflex activity is present
which maintain respiration and the circulation. The patient
responds neither to intense pain, nor verbal stimuli.
c. What is the meaning of Yantok losing his consciousness since 1 hour
ago?
Answer:
Yantok has a heat stroke results from exposure to a high
environmental temperature. Heat stroke should be considered in any
patient whose core temperature is elevated significantly (>104°F
[40°C]) and who has mental status changes such loss of
consciousness. The most commonly used definition of heat stroke
worldwide is the Bouchama’s definition. Bouchama has defined heat
stroke as a core body temperature that rises above 40 °C,
accompanied by hot dry skin and central nervous system
abnormalities, such as delirium, convulsions, or coma (Hifumi,
2013).
d. What is the pathophysiology of losing consciousness since 1 hour
ago?
Answer:
The influence of the sun on the heat regulatory center increased
body metabolism have each been held responsible for the
breakdown in the heat regulatory mechanism and for the clinical
manifestations in heat stroke. The pathophysiology is heat transfer
mechanisms are overwhelmed and central thermoregulatory control
is ineffective. Consequently, the core temperature can rise quickly to
injurious levels. Heat stroke arises when cellular injury is caused by
excess body temperature. If the core temperature rises above 105.8°F
(41°C) for more than a short time, thermal injury results. Proteins are
denatured, and injured cells undergo apoptosis (programmed cell
death) or necrosis. Even before injury takes place, an individual may
suffer transient mental and physical impairment, such as losing
consciousness (Jardine, 2017).
e. What is the impact of losing consciousness in this case?
Answer:
Impact of losing consciousness according to Grauwmeijer in 2018,
are:
a. Coma
Coma is a pathological state marked by severe and prolonged
dysfunction of vigilance and consciousness (at least 1 hour).
b. Convulsion
c. Cognitive decline
d. Dysregulation of emotional expression
e. Death of neurons and brain cells
f. Death
2. Two hours ago, Yantok was suffered general convulsion during five
minutes. At 9 am, Yantok brought by his mother when queue “sembako”
at Monpera. Yantok began sweating and felt warm in whole body at 12
pm when the wheater was sweltering.
a. What is the meaning of two hours ago Yantok was suffered general
convulsion during five minutes?
Answer:
The meaning of two hours ago Yantok was suffered general
convulsion during five minutesis yantok experience Rapid onset of
hyponatraemia can lead to altered conscious level and seizure caused
by heat stroke in this case. Hyperthermia associated with the acute
physiological alterations predominant central nervous system
dysfunction resulting in convulsion (Leon, 2015; Burt, 2016).
b. What is the correlation between two hours ago Yantok was suffered
general convulsion during five minutes with loss of consciousness in
the next hour?
Answer:
Correlation between two hours ago Yantok was suffered from
general convulsion during five minutes with loss of consciousness in
the next hour is Yantok undergone progression of central nervous
system dysfunction.
c. What is the classification of convulsion?
Answer:
According to ILEA in 2018, the classification of convulsion are:
a. Focal aware seizures
Previously called partial seizures. In these seizures the person is
conscious (aware and alert), will usually know that something is
happening and will remember the seizure afterwards.
b. Focal impaired awareness seizures 
Previously called complex partial seizures. In these seizures the
person’s consciousness is affected and they may be confused.
They might be able to hear you, but not fully understand what
you say or be able to respond to you. 
c. Generalised onset seizures
These seizures affect both sides of the brain at once and happen
without warning.
d. Tonic clonic seizures
The seizure most people will recognise, where a person will jerk
and shake as their muscles relax and tighten.
e. Atonic seizures (sometimes called drop attacks) and tonic
seizure
In an atonic seizure the person’s muscles suddenly relax and
they become floppy, and they oftern fall, usually forwards. In a
tonic seizure the person's muscles suddenly become stiff and
they often fall, usually backwards.
f. Myoclonic seizures
Myoclonic means ‘muscle jerk’. Muscle jerks are not always
due to epilepsy (for example, some people have them as they
fall asleep).
g. Absence seizures
Absence seizures (previously called petit-mal) are typical
absences or atypical absences. During a typical absence the
person becomes blank and unresponsive for a few seconds.
Atypical absences are similar to typical absences but they start
and end more slowly, and last a bit longer.
d. What is the pathophysiology of convulsion?
Answer:
Queque 4 hour when the weather was sweltering makes the body
gaining heat that leads to abnormality physiologic condition, heat
gain is counteracted by a commensurate heat loss. This is
orchestrated by the hypothalamus , which function as a thermostat.
When heat gain exceed heat loss, the body temperature rises, but the
body can’t compensation, hyperthermia occurs. In hyperthermia
condition , basal metabolism increased, the need for oxygenand
glucose increases causing disruption of normal function Na⁺ and
reuptake glutamate acid by glia cells . the concentration of natrium
in intracellular is increasing because of the neuron membrane cells
are permeability to natrium . as the effect ofnatrium intracellular
increased, there is changes in the potential neuron membrane cells.
Membrane cells in depolarization state causing many ion releases
and damaging GABA–nergic neuron. Inhibitory function disturbed
and continuous release of ca+ causing convulsion (Silbernagl, 2014).
e. What is the impact of general convulsion?
Answer:
According to Pediatric Guidelines in 2006, impacts of general
convulsion are:
a. Epilepsy
b. Hypoglycaemia
Convultion may be a presenting sign
c. Pebrile convulsions
d. Hypoxia
e. Hypotensions
f. What is the meaning of Yantok began sweating and felt warm in
whole body at 12 pm when the wheater was sweltering?
Answer:
Yantok is in homeostatic state when the body is hot the
thermoregulator system will try to reduce heat by dilated blood
vessel and stimulate ekrin gland to exreting sweat.
g. What is the correlation between Yantok began sweating and felt
warm in whole body at 12 pm when the wheater was sweltering with
chief complaint?
Answer:
Sweating is body’s compensations towards high temperature before
the central nervous system dysfunction. When body cannot
compensate anymore, it later leads to loss of consciousness. There
might be correlation between profuse sweating and loss of
consciousness due to dehydration.
h. How is the mechanism of sweating?
Answer:
The process of sweating is regulated by the hypothalamus. the
hypothalamus can produce a bradykinin enzyme that affects the
sweat glands. if the hypothalamus gets stimulation, such as changes
in temperature in the blood vessels, then the stimulus will be
forwarded by the sympathetic nerves to the sweat glands. then the
sweat glands will absorb the brine and a little urea from the
capillaries and then send it to the surface of the skin in the form of
sweat. Sweat will evaporate and absorb body heat so that body
temperature remains constant (Guyton, 2014).
i. What are the possible causes of general convulsion in this case?
Answer:
Since the chief means of heat dissipation are radiation, conduction
and convection, and evaporation from the skin, various explanations
involving the breakdown of these mechanisms have been proposed
as the primary cause for heat stroke. Reasons for convulsions
according to Shelley in 2017, are:
a. Most convulsions in children under the age of 5 years will be
due to febrile convulsions (these tend to occur in children 6
months and 5 years).
b. Epilepsy
c. Hypoglicaemia
d. Hypoxia
e. Hypotension
j. What is the meaning of standing in hot weather for 4 hours?
Answer:
It would be the risk factor of heat stroke. Heat stroke results from
exposure to a high enviromental temperature (in which case it is
called classic or nonexertional heat stroke) (Bouchama, 2003).
3. Physical Examination: Primary Survey.
a. What is the interpretation of primary survey?
Answer:
Table 2.2. Primary Survey.
Examination Normal Case Interpretation
Airway No snoring No snoring Normal

Breathing RR: 16- RR: 32x/minutes Tachipnea


24x/minutes
No rales, no No rales, no Normal
wheezing wheezing

Circulation BP: 120/80 BP : 90/70 Hypotension


mmHg mmHg

PR: 100x/minutes PR : Tachicardia


140x/minutes

Capillary refilled Capillary refilled Indicate


time < 2 second time < 3 second dehydration

Dissability Eyes opening Eye : 2


response to pain. Movement : 5
Best motore Verbal :3
response move (GCS :10 
to localized pain. Moderate head i
Best verbal injury)
response
inappropriate
words
Sight reflex (+) Normal

Exposure Temp. 36,5 – Temp. 41oC Hyperpirexia


37,5oC
b. What is the mechanism of primary survey?
Answer:
a. Tachypnea and tachycardia
Queque 4 hour when the weather was sweltering can cause the
body gaining heat. When heat gain exceed heat loss, it leads to
hyperthermia as a result of basal metabolism rising which
makes the need for oxygen increased. As a result, tachypnea and
tachycardia occur.
b. Dehydration
Queque 4 hour when the weather was sweltering can cause the
body gaining heat. Thermosensor located in the skin, muscles,
and spinal cord send information regarding the core body
temperature to anterior hypothalamus. The sympatethic
responses increasing cardiac output and blood flow to the skin
induces dilatation of pheriphal venous system and stimulation of
the eccrine sweet glands to produre sweat (evaporation) which
can cause an inadequate extracellular flui that intracellular fluid
are shifting into extracellular. Later, the cells in hypotoni
condition which leads to dehydration.
c. Moderate Head Injury
Queque 4 hour when the weather was sweltering can cause the
body gaining heat cause thermosensor located in the skin,
muscles, and spinal cord send information regarding the core
body temperature to anterior hypothalamus. Overwhelmed heat
gain than loss the cause dysfunction of central nervous system
which leads to moderate head injury. There might also be
correlation between CNS dysfunction and dehydration.
Synthesis:
A normal body temperature is maintained at approximately 37
°C by the anterior hypothalamus through the process of
thermoregulation. Several mechanisms related to sweating, such as
vaporization, radiation, convection, and conduction, function to cool
the body surface. As the body temperature increases, active
sympathetic cutaneous vasodilation increases blood flow in the skin
and initiates thermal sweating. Cutaneous vasodilation causes a
relative reduction in intravascular volume, leading to heat syncope.
The loss of salts and water through sweat induces dehydration and
salt depletion, which are associated with heat exhaustion and cramps
unless appropriate supplementations of water and salt are initiated.
Further loss of salt and water impairs thermoregulation followed by
the reduction of visceral perfusion due to shunt from the central
circulation to the skin and muscles, resulting in organ failure.
Therefore, heat stroke is a condition of multiple organ failure caused
by hot environment (Hifumi, 2018).
The mechanism of how body react to warm environment is
started when heat is received through skin. The stimulus of heat
begins to travel through receptor, to the nerves before entering the
dorsal root ganglion. From dorsal root ganglion, neuron activated by
glutamate through lateral prebrachial dorsal where the activation of
thermoregulatory warm afferent occur. The activated excitatory
neuron continues the transmission through preoptic area. In medial
preoptic area, the activated inhibitory neuron plays a role using
GABA as neurotransmitter. Later, the impuls processed in
dorsomedial hypothalamus. Next, the feedback mechanism is
transmitted through rostral medullary raphe region before
transmitted to ventral root ganglion and arrive at the effector such as
skin and endothelial tissues where it dilates (Dunn, 2017).
Figure 1. Mechanism of body response towards warm environment.
Source: Dunn, 2017.

Core body temperature is maintained by the body’s ability to


balance heat exposure and heat production with heat dissipation to
the environment. Heat related illness occurs when the body is unable
to regulate its core temperature in response to excess heat exposure
and heat production, coupled with decreased heat dissipation.
The body uses the mechanism of heat dissipation to balance
the effects of excess heat exposure (environmental heat) or excess
heat production (exertion). Effective heat dissipation depends on the
rapid transfer of heat from the core of the body to the skin and from
the skin to the external environment. There are 4 mechanisms of
heat dissipation: radiation, evaporation, convection, and conduction.
Under normal physiologic conditions, radiation and evaporation
account for most heat transfer in humans.
a. Radiation involves heat transfer through infrared rays. It occurs
when the environmental temperature is below body temperature,
and it accounts for 65% of heat transfer under normal
physiologic conditions. Once the environmental temperature
reaches 35°C (95°F), radiation becomes less effective. When the
environmental temperature exceeds body temperature, heat is
gained instead of lost.
b. Evaporation involves heat transfer through the conversion of
sweat from liquid to gas at the skin surface, and it is the main
mechanism of heat dissipation at higher environmental
temperatures, when radiation is less effective. When the
humidity level exceeds 75%, heat transfer by evaporation begins
to decrease.
c. Convection involves heat transfer through the movement of air
or water over the skin surface. Under normal physiologic
conditions, about 10% of heat transfer occurs by convection.
d. Conduction involves heat transfer through physical contact of
the body with another cooler surface or object. Conduction
allows for approximately 2% of heat loss under normal
physiologic conditions.
As the environmental temperature increases, the body's
ability to dissipate heat through radiation decreases, and
convection and evaporation gain greater importance in preventing
heat-related illness. Convection and evaporation are directly
controlled by circulatory dynamics and sweating. The
hypothalamus compensates for each 1°C (1.8°F) increase in core
temperature by promoting cutaneous vasodilatation and increasing
the rate of sweating. Vasodilatation dissipates heat by convection,
and sweat dissipates heat by evaporation.
It has been postulated that children are at increased risk for
heat-related illness due to several physiologic reasons. These
include greater body surface area-to-body mass ratio, production
of more metabolic heat per kilogram of body weight, a slower rate
and volume of sweat production, a higher temperature required to
stimulate the sweating mechanism, and a lower cardiac output at a
given metabolic rate. In extreme environmental conditions,
children may thermoregulate less effectively (Dunn, 2017).
c. What kind of disorder is associated with general flushing?
Answer:
According to Izikson et al in 2006, flushing is the body’s way of
responding to many everyday conditions or normal body states
including:
a. Alcohol consumption
b. Exercise
c. High environmental temperatures
d. Medication side effects
e. Menopause
f. Pregnancy
g. Rapid changes in temperature
h. Sexual arousal
i. Spicy foods
j. Strong emotions
Flushing can also be caused by medical conditions that are localized
to the skin or may affect the entire body including:
a. Carcinoid syndrome (group of symptoms caused by a tumor that
secretes hormones and other biologically active substances)
b. Polycythemia (increased amount of circulating red blood cells)
c. Fever
d. Heat stroke or heat exhaustion
e. Hyperthyroidism (overactive thyroid)
f. Mastocytosis (accumulation of a type of inflammatory cells,
called mast cells, in body tissues)
d. What are the manifestations of dehydration?
Answer:
According to King in 2003, manifestations of dehydration are in
table below.
Table 2.3. Manifestations of Dehydration.
Mild (< 3% body Moderate (3-9% Severe (>9% body
Symptom
weight lost) body weight lost) weight lost)
Restless or fatigued, Apathetic, lethargic,
Mental status Normal, alert
irritable unconscious
Tachycardia or
Heart rate Normal Normal to increased
bradycardia
Weak, thready,
Quality of pulse Normal Normal to decreased
impalpable
Tachypnea and
Breathing Normal Normal to increased
hyperpnea
Eyes Normal Slightly sunken Deeply sunken
Fontanelles Normal Slightly sunken Deeply sunken
Tears Normal Normal to decreased Absent
Mucous
Moist Dry Parched
membranes
Skin turgor Instant recoil Recoil < 2 seconds Recoil >2 seconds
Capillary refill < 2 seconds Prolonged Minimal
Extremities Warm Cool Mottled, cyanotic

4. Physical Examination: Secondary Survey.


a. What is the interpretation of secondary survey?
Table 2.4. Secondary Survey.
Examination Normal Interpretation
Head: Moist Sign of dehydration
Mouth: dry lips
Upper and lower Sign of heat stroke
extremities:
Hot and flushing
b. What is the mechanism of secondary survey?
Answer:
a. Dry lips
Heat from outside received by thermoreseptor in skin transmitted
as stimulus anterior hypthalamus which has effect on sympathrtic
nerves that induces sweat glands cause sweating. The profuse
sweating can cause lost of H2O throught evaporation which leads
to dehydration which of its sign is dry lips.
b. Upper and Lower extremities: hot and flushing.
Heat from outside received by thermoreseptor in skin transmitted
as stimulus anterior hypthalamus which has effect on sympathrtic
nerves that induces vasadilatation of blood vessel which can
cause blood flow increase to the skin. Later, hot and flushing
extremities occur.
Synthesis:
Two centers for temperature regulation are in the hypothalamus. The
posterior region, activated by cold, triggers reflexes that mediate
heat production and heat conservation. The anterior region,
activated by warmth, initiates reflexes that mediate heat loss. In the
process of thermoregulation, skin blood fl ow can vary
tremendously, from 400 ml/min up to 2500 ml/min. The more blood
that reaches the skin from the warm core, the closer the skin’s
temperature is to the core temperature. The skin’s blood vessels
diminish the effectiveness of the skin as an insulator by carrying heat
to the surface, where it can be lostfrom the body by radiation and
conduction-convection. Accordingly, skin arteriolar vasodilation,
which permits increased flow of heated blood through the skin,
increases heat loss. Conversely, skin vasoconstriction, which reduces
skin blood flow, decreases heat loss by keeping the warm blood in
the central core, where it is insulated from the external environment.
This response conserves heat that otherwise would have been lost
(Sherwood, 2011).
5. How to diagnose?
Answer:
A. Anamnesis :
1. Loss of consciousness since 1 hour.
2. Convulsion during 5 minutes before loss of consciousness.
2. Yantok standing in sweltering weather for 4 hour.
B. Physical Examination
1. Primary Survey
a. BP : 90/70mmhg, Pulse Rate 140x/minutes with hot
extremities and capillary refilled time < 3 second
b. RR : 32x/minutes
c. GCS 9
d. Temperature 41oC and General Flushing.
2. Secondary Survey
a. Mouth : Dry Lips.
b. Extremities : Hot and Flushing.
Synthesis:
When a patient presents with signs and symptoms of a heat-related
illness, there are certain key questions the emergency clinician should ask
when taking the history. Has the patient been involved in exertional
activities in a hot or humid environment? Is the patient new to the
physical activity? Is the patient taking any type of stimulant medication,
either prescribed or recreational? How long has the patient been exposed
to heat?
The physical examination in a suspected heat-related illness should
be problem-focused. The emergency clinician needs to be observant of
vital signs, and abnormal vital signs should be addressed. Either rectal or
esophageal temperature should be obtained to estimate core temperature,
as all other external temperatures are inadequate at predicting core
temperature and may be falsely depressed. Poor prognosis is likely if the
patient's core temperature is > 42°C (107.6°F).
A neurologic examination and Glasgow Coma Scale (GCS) score
will not only allow the emergency clinician to address the severity of the
injury and diagnose heat stroke, but also to determine the need for
immediate intervention and resuscitation. A cardiac examination should
be completed to evaluate for tachycardia and/or dysrhythmias and to
evaluate for adequate perfusion. An increase or decrease in respiratory
effort can be a presenting abnormality in heat-related illness. Both
profuse sweating or a lack of sweating can provide necessary information
to the emergency clinician that a patient may have a heat-related illness.
The diagnosis of heat stroke is based on clinical symptoms and
does not require any laboratory abnormalities. Laboratory test results for
patients with heat stress or heat exhaustion are usually normal or
consistent with dehydration; other organ systems are usually not
involved. Nonetheless, heat stroke has been found to be associated with
multisystem organ dysfunction as well as myocardial injury, so although
diagnostic studies are not needed to verify the diagnosis and should not
delay immediate treatment, diagnostic studies may assist with managing
complications associated with a heat-related illness. In patients with heat
stroke, laboratory tests can reveal an elevated lactate level from poor
perfusion. In addition, hepatic injury is a common finding in patients
with heat stroke. Aspartate aminotransferase (AST) and alanine
aminotransferase (ALT) elevations peak approximately 48 to 72 hours
after exposure to heat and gradually return to normal in 10 to 14 days.
Elevation of bilirubin levels as well as prothrombin time have been
reported secondary to liver injury.
Rhabdomyolysis with an elevated creatine kinase can be associated
with heat-related illness. Acute renal injury leading to renal failure can
also occur with heat stroke, but it generally responds well to rehydration
and usually corrects in a few days. Hematologic findings can include
anemia from red blood cell membrane osmotic fragility.
Thrombocytopenia and findings of disseminated intravascular
coagulation with prolongation of prothrombin time, partial
thromboplastin time, and D-dimer are also found with heat stroke (Dunn,
2017).

6. What are the differential diagnoses?


Answer:
The differential diagnoses in this case are:
a. Exertional heat stroke (EHS)
EHS is characterized by hyperthermia, diaphoresis, and an
altered sensorium, which may manifest suddenly during extreme
physical exertion in a hot environment. A number of symptoms (eg,
abdominal and muscular cramping, nausea, vomiting, diarrhea,
headache, dizziness, dyspnea, weakness) commonly precede the heat
stroke and may remain unrecognized. Syncope and loss of
consciousness also are observed commonly before the development
of EHS.
EHS commonly is observed in young, healthy individuals (eg,
athletes, firefighters, military personnel) who, while engaging in
strenuous physical activity, overwhelm their thermoregulatory
system and become hyperthermic. Because their ability to sweat
remains intact, patients with EHS are able to cool down after
cessation of physical activity and may present for medical attention
with temperatures well below 41°C. Despite education and
preventive measures, EHS is still a leading cause of disability and
death in high school athletes, particularly football players.
Risk factors that increase the likelihood of heat-related
illnesses include a preceding viral infection, dehydration, fatigue,
obesity, lack of sleep, poor physical fitness, and lack of
acclimatization. Although lack of acclimatization is a risk factor for
heat stroke, EHS also can occur in acclimatized individuals who are
subjected to moderately intense exercise. EHS also may occur
because of increased motor activity due to drug use, such as cocaine
and amphetamines, and as a complication of status epilepticus.
b. Non- Exertional heat stroke
NEHS is characterized by hyperthermia, anhidrosis, and an
altered sensorium, which develop suddenly after a period of
prolonged elevations in ambient temperatures (ie, heat waves). Core
body temperatures greater than 41°C are diagnostic, although heat
stroke may occur with lower core body temperatures.
Numerous central nervous system (CNS) symptoms, ranging
from minor irritability to delusions, irrational behavior,
hallucinations, and coma have been described. Other possible CNS
symptoms include seizures, cranial nerve abnormalities, cerebellar
dysfunction, and opisthotonos. Anhidrosis due to cessation of
sweating is a late occurrence in heat stroke and may not be present
when patients are examined.
Patients with NEHS initially may exhibit a hyperdynamic
circulatory state, but, in severe cases, hypodynamic states may be
noted. Classic heat stroke most commonly occurs during episodes of
prolonged elevations in ambient temperatures. It affects people who
are unable to control their environment and water intake (eg, infants,
elderly persons, individuals who are chronically ill), people with
reduced cardiovascular reserve (eg, elderly persons, patients with
chronic cardiovascular illnesses), and people with impaired sweating
(eg, from skin disease or ingestion of anticholinergic or psychiatric
drugs). In addition, infants have an immature thermoregulatory
system, and elderly persons have impaired perception of changes in
body and ambient temperatures and a decreased capacity to sweat.
Synthesis:
Heat-related illness occurs along a continuum from heat stress, to
heat exhaustion, to heat stroke. The signs and symptoms of the different
stages of the illness can overlap.
a. Heat stress is characterized by perceived discomfort and physiologic
strain, including heat cramps, while a normal core temperature is
maintained.
b. Heat exhaustion is characterized by a rise in body temperature
usually associated with dehydration, with a core body temperature <
40°C (104°F). Signs and symptoms of heat exhaustion include
fatigue, weakness, dizziness, nausea, vomiting, myalgias, profuse
sweating, intense thirst, tachycardia, syncope, and headache, with the
absence of severe neurological symptoms.
c. Heat stroke is a life-threatening failure of thermoregulation
characterized by a body temperature ≥ 40°C (104°F), with central
nervous system abnormalities such as confusion, convulsions, or
coma. It is associated with severe dehydration, endotoxemia,
circulatory failure, and, potentially, multisystem organ failure.
It is imperative that the emergency clinician be able to differentiate
hyperthermia from fever. In hyperthermia, the hypothalamus has a
normal set point and the body is unable to dissipate enough heat to match
the set point, resulting in an elevated core temperature. In contrast, fever
occurs when the hypothalamic set point is increased by circulating
cytokines, and the body attempts to conserve and generate heat until the
core temperature rises to the new set point. The differential diagnosis of
heat-related illness includes any disease process that causes hyperthermia
from excess heat exposure or production. Causes of hyperthermia include
toxins and associated toxidromes such as anticholinergic and serotonin
syndromes. Another drug-related cause of hyperthermia includes
neuroleptic malignant syndrome, most notably associated with
antipsychotic drugs. Malignant hyperthermia is an autosomal-dominant
condition that results in an elevation in core temperature following
exposure to medications such as inhalational anesthetic agents and
paralytic agents, and it causes skeletal muscle rigidity and a rapid
increase in core temperature. There are similarities between exertional
heat stroke and malignant hyperthermia; although the inciting etiology is
different, both lead to excessive heat production. A thorough history of
exposures will lead to easy differentiation between these diseases.
According to Wahab in 2016, other possible diagnosis with features
of hyperthermia and CNS dysfunction must be ruled out based on focus
history and clinical assessment of the patient:
1. Intrinsic Factors
a. Central nervous system (CNS) injury
b. Hyperthyroid storm
c. Infection /Septicemia
d. Neuroleptic malignant syndrome (NMS)
2. Extrinsic Factors
a. Anticholinergic poisoning
b. Drug ingestion
c. Heat exhaustion

Figure 2. Heat related illness classification.


Source: Hifumi, 2018.
7. What are additional examinations needed in this case?
Answer:
Some additional examinations needed in this case according to Miyake in
2013, are:
a. Laboratory examination in some cases may indicate
hemoconcentration (increased hematocrit) and hyponatremia (if
sodium depletion becomes a primary problem).
b. Arterial blood gas analysis may indicate a state of metabolic
acidosis.
c. If circumstances persist, laboratory tests may indicate the presence
of heart failure and other complications.
Synthesis:
The electrolyte abnormalities that occur in HS have been well
described in patients with EHS. It is thought that a similar picture is
seen in NEHS. Hypercalcaemia and hyperalbuminaemia may develop
secondary to dehydration.
Hypokalaemia and hypophosphataemia are common early in the
course of HS and are thought to be secondary to the combined effects of
losses in sweat, the effects of catecholamines and hyperventilation.
Hyperkalaemia and uraemia may follow later and renal replacement
therapy may be indicated. Continued damage to tissue cells causes
leakage of phosphate into the extracellular space. Here it may bind to
calcium causing hypocalcaemia and hyperphosphataemia.
Renal injury in HS is multifactorial. Hypovolaemia,
rhabdomyolysis and disseminated intravascular coagulation are all
potential contributing factors. Creatinine kinase levels are elevated in
both EHS and NEHS although they are higher in the former. Differing
rates for the prevalence of acute kidney injury have been reported, with
AKI occurring more frequently in EHS than NEHS.
Tachypnoea leads to an increased minute volume and arterial
blood gas sampling may reflect this. In EHS there is initially a
respiratory alkalosis. This may progress to a metabolic acidosis and
hyperlactataemia secondary to sustained tissue damage. In contrast,
patients with NEHS classically present with a respiratory alkalosis
alone. Severe cases of either type of HS can present with pulmonary
oedema, pulmonary infarction or acute respiratory distress syndrome
requiring sedation, intubation and commencement of mechanical
ventilation.
Polycythaemia is commonly seen due to dehydration. Cellular
metabolism and enzymatic reactions are affected at temperatures
between 42-44°C.5,8 This includes direct activation platelets leading to
microthrombosis. A consumption coagulopathy can occur, which in
turn, can lead to excessive bleeding. Presence of a consumption
coagulopathy is an indicator of poor prognosis (Adam, 2016).

Table 2.5. Suggested Diagnostic Studies.


Organ system Diagnostic studies
Circulatory Basic metabolic panel, lactate
Cardiac Troponin, CK, ECHO, ECG
Hepatic AST, ALT, bilirubin, PT, PTT, INR
Renal BUN, Cr, UA
Hematologic CBC, PT, PTT, INR, D-dimer
Musculoskeletal CK, urine myoglobin
Neurologic Heat CT
Source: Dunn, 2017.

8. What is the working diagnosis of this case?


Answer:
Nonexertional Heat Stroke (NEHS) with moderate-severe dehydration.

9. What is the comprehensive management needed for this case?


Answer:
Patients with suspected heat stroke should have a rapid assessment of the
adequancy of airway, breathing, circulation and neurological status. The
mainstays of treatment after alternative diagnose have been ruled out is
rapid cooling. Cooling methods is to rapidly dissipate heat from the
body’s core to the external environment without causing cutaneous
vasoconstriction or shivering. There are two phase of treatment
according to Bouchama in 2007, which are:
a. Pre hospital treatment: where possible, the patient should cease all
activity, be moved into the shade, have any excess clothing removed,
be sprayed with water and continuously fanned. Ice packs should be
applied to the neck, axilla annd groins.
b. Intrahospital treatment: Immediate administration of
benzodiazepines is indicated in patients with agitation and shivering,
to stop excessive production of heat. In addition, benzodiazepines
are the sedatives of choice in patients with sympathomimetic-
induced delirium as well as alcohol and sedative drug withdrawals.
Dose of diazepam in child 3-<5 years (14-19 kg)1,5ml per rectal.
Synthesis:
According to Dunn in 2017, comprehensive management needed for heat
stroke can be divided into two, which are:
A. Prehospital Care
Prior to emergency medical service (EMS) provider arrival,
prehospital care for a patient with exertional heat-related illness may
include immediate care provided by coaches and athletic trainers on
the scene. Once a heat-related illness is suspected, the patient should
be removed from the environmental heat source and placed in a cool,
shaded area. If applicable, the equipment, uniform, or clothing
should be removed and oral rehydration initiated while waiting for
EMS arrival. If available, rapid cooling with immersion in a tub of
ice water should be considered.
Basic Life Support (BLS) interventions for patients with heat-
related illness include immediate assessment of airway, breathing,
and circulation (ABC). After initial assessment of the ABCs, the
BLS unit should remove the patient’s clothing (if not already done),
obtain a rectal temperature, if possible, and begin cooling
interventions. If Advanced Life Support (ALS) medical providers are
available, additional interventions include performing an
electrocardiogram with interpretation, placing an advanced airway, if
indicated, administering intravenous (IV) fluids, and managing
seizure activity. Prompt and appropriate prehospital care can greatly
improve patient outcomes. If transportation is prolonged, immediate
cooling measures should be considered.
B. Treatment
The initial care of the patient with a heat-related illness should
focus on evaluation and support of the ABCs. Dehydration is often
associated with heat-related illness and attention should be given to
adequate fluid resuscitation. As heat-related illness progresses,
attention to complications associated with heat exhaustion and heat
stroke need to be addressed, including electrolyte abnormalities,
multisystem organ failure, disseminated intravascular coagulation,
seizures, and coma.
The key to management is the initiation of rapid cooling,
because morbidity and mortality are directly related to the duration
and intensity of the hyperthermia. A retrospective study concluded
that hyperthermic patients with a higher initial temperature,
hypotension, or a low GCS score had a higher mortality rate.
Decreasing the temperature to below 40°C (104°F) is critical and
more important than how high the initial temperature was.
The most-recommended methods of cooling utilize the
property of heat dissipation. When core temperatures are high,
cooling measures utilizing the properties of conduction and
evaporation are used to rapidly decrease the core temperature.
1. Conductive Cooling
Cooling measures using conductive heat dissipation
include water immersion, ice pack application, cooling blankets,
and more-invasive iced peritoneal or gastric lavage. With water
immersion, the patient is submerged into either cold water or ice
water. With ice water, a steeper temperature gradient can be
obtained and can potentially increase the rate of heat dissipation,
but it is postulated that aggressive cooling with ice water may
secondarily cause shivering and peripheral vasoconstriction,
thereby impeding the efficacy of ice-water immersion. Despite
study found that 12 minutes of immersion in either ice or water
was more effective than passive cooling, but the cooling rates
were similar for immersion in ice or water.
Monitoring vital signs and temperature can be difficult
with water immersion; therefore, this can be a challenge to
perform in the ED setting. Practically, the lack of a tub can also
prevent this treatment in the ED, but this method of cooling can
be considered on-scene for patients with hyperthermia, such as a
football locker room or sporting event treatment unit. Ice-water
immersion is best utilized with a patient who is awake and alert,
but it can be performed with patients with altered mental status.
Ice-pack application usually involves placing ice packs
over the large vessels of the body, such as the neck, axillae, and
groin. Study found greater blood flow over the chest and back of
boys with heat exposure, which suggests that other potential
sites for ice application should include the chest and back. Ice-
pack cooling promotes heat exchange adjacent to areas of
increased blood flow by convection and conduction, but used
alone, it is not as effective as other cooling measures. Indeed,
evaporative cooling was found to have a higher cooling rate
compared to ice packs. The least effective of all conductive
cooling measures is probably cooling blankets.
2. Evaporative Cooling
The most recognized and recommended method of cooling in
the ED setting is evaporative cooling. Evaporative cooling
requires all clothing to be removed from the patient, followed by
spraying water over the skin in a setting where there is
continuous airflow. Study suggested that a warm environment is
crucial for the evaporative process, which can be accomplished
with either warm forced air and/or by warming the water
sprayed on the body. As an alternative method of evaporative
cooling, a sheet wetted with tap water and placed over the body
in a setting with fans was as effective as spraying warm water.
3. Cooled Fluid Administration/Lavage
Historically, cooled IV normal saline (0.9%) or iced
lavage fluids have been used as conductive cooling methods to
reduce core temperature in patients with heat-related illness.
There is no literature to support the use of cooled IV saline for
the treatment of hyperthermia in children, and this method is
associated with discomfort and shivering. Studu showed that, in
patients who received cold normal saline, high-dose diazepam
(20 mg) compared to low-dose diazepam (10 mg) or placebo
control showed improved reduced core body temperature
without oxygen consumption or shivering. There are no human
studies that compare iced gastric or bladder lavage to other
cooling measures; however, studies in animals have shown
mixed results. Iced gastric lavage was studied in a canine model
and yielded a cooling rate that was 5 times faster than controls
in ambient air temperature; (0.15°C/min vs 0.03°C/min). In
another canine experiment, iced gastric lavage was not
advantageous compared to evaporative cooling.
Due to the lack of evidence for the use of cooled IV or
iced lavage fluids, it is not routinely recommended for heat-
related illness, but consideration should be given to its use in
children with severe heat stroke. No studies have evaluated the
effect of more-invasive cooling measures (such as peritoneal or
thoracic lavage) in the treatment of heat-related illness in
children; therefore, they are not recommended for the
management of heat-related illness, as they are invasive, time
consuming, and difficult to perform.
Pharmacologically induced cooling measures have little
role in the management of heat-related illness. Due to the
normal set point of the hypothalamus and the pathophysiology
associated with heat-related illness, antipyretics should not be
used in the treatment of hyperthermia, as the etiology of the
hyperthermia with heat-related illness is not related to
circulating cytokines. However, benzodiazepines can be
considered to decrease shivering if cooled IV fluids are used for
a patient with heat stroke.
Figure 3. Clinical pathway for management.
4. What are the complications of this case?
Answer:
The most serious complication of heat stroke is the occurrence of
multiorgan dysfunction syndrome. including encephalopathy,
rhabdomyolysis, acute renal failure, acute respiratory distress syndrome,
myocardial damage, hepatocellular damage, ischemia, or intestinal
infarction, pancreatic damage, and bleeding complications, especially
intravascular disseminatory coagulation with clear thrombocytopenia
Death can occur due to complications of heart failure, renal failure,
intravascular coagulation dissemination, and rhabdomyolysis (Grogan
and Hopkins, 2012; Widjojo, 2015).

5. What is the prognosis of this case?


Answer:
Quo ad vitam : Bonam
Quo ad fungsionam : Dubia ad Bonam
Synthesis:
Patients who have mild heat stroke generally recover uneventfully.
There usually are no sequelae, and neurologic functioning is intact when
tested several months later. Those who survive moderate-to-severe heat
stroke have a good chance of making an intact recovery, but the risk of
sequelae is higher. If the core temperatures have been greater than
107.6°F (42°C), patients have a poorer prognosis. The prognosis is
optimal when HS is diagnosed early and management with cooling
measures and fluid resuscitation and electrolyte replacement begins
promptly. The prognosis is poorest when treatment is delayed >2 hours.
Heat stroke must be viewed as multisystem failure. CNS injury is
permanent in 20 percent of cases and is associated with poor prognosis.
Rhabdomyolysis caused by tissue destruction is common and results in
myoglobinuria and risk of renal injury.

6. How does the competence of general practitioner for this case?


Answer:
The competence of general practitioner for this case is 3B, an emergency
case.

7. How does Islamic point of view for this case?


Answer:
“It is He who expelled the ones who disbelieved among the People of the
Scripture from their homes at the first gathering. You did not think they
would leave, and they thought that their fortresses would protect them
from Allah ; but [the decree of] Allah came upon them from where they
had not expected, and He cast terror into their hearts [so] they destroyed
their houses by their [own] hands and the hands of the believers. So take
warning, O people of vision.” (QS. Al Hashr 59:2)

“Rather, man, against himself, will be a witness. Even if he presents his


excuses.” (QS. Al-Qiyamah 75:14-15).

5.3 Conclusion
Yantok, 4 years old boy, suffered from convulsion and loss of consciousness
caused by nonexertional heat stroke and moderate-severe dehydration.

5.4 Conceptual Framework

High Temperature General flushing


Activation of Sympathetic endothel
thermoregulation in and cutaneus
hypothaamus vasodilatation

Hypothalamus cannot Profuse sweating


compensate

CNS dysfunction Moderate-severe


dehydration

Convulsion Loss of consciousness

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