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).
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