کمک های اوليه در اختلالات دمایی و برق

گرفتگی

دکتر شهيده امينی هيات علمی گروه داروسازی بالينی

گرمازدگی

Hyperthermia Heat Stroke Heat illness

Body temperature is controlled by the hypothalamus. Neurons in both the preoptic anterior hypothalamus and the posterior

hypothalamus receive two kinds of signals: one from peripheral nerves that transmit information from

warmth/cold receptors in the skin and the other from the temperature of the blood bathing the region.

These two types of signals are integrated by the thermoregulatory center of the hypothalamus to maintain normal temperature.

In a neutral temperature environment, the metabolic rate of humans produces more heat than is necessary to maintain the core body temperature in the range of 36.5–37.5°C .

Hyperthermia

Hyperthermia is defined as elevation of core body temperature above the normal diurnal range of 36 to 37.5ºC due to failure of thermoregulation.

Fever versus Hyperthermia

Fever is an elevation of body temperature that exceeds the normal daily variation and occurs in conjunction with an increase in the hypothalamic set point (e.g., from 37°C to 39°C ).

Once the hypothalamic set point is raised, neurons in the vasomotor center are activated and vasoconstriction commences. The individual first notices vasoconstriction in the hands and feet. Shunting of blood away from the periphery to the internal organs essentially decreases heat loss from the skin, and the person feels cold. For most fevers, body temperature increases by 1°–2°C.

Shivering, which increases heat production from the muscles, may begin at this time; however, shivering is not required if heat conservation mechanisms raise blood temperature sufficiently. Nonshivering heat production from the liver also contributes to increasing core temperature.

Heat loss

Heat load

Hyperthermia

Hyperthermia is characterized by an uncontrolled increase in body temperature that exceeds the body's ability to lose heat.

The setting of the hypothalamic thermoregulatory center is unchanged. In contrast to fever in infections, hyperthermia does not involve pyrogenic molecules .

Exogenous heat exposure and endogenous heat production are two mechanisms by which hyperthermia can result in dangerously high internal temperatures. Excessive heat production can easily cause hyperthermia despite physiologic and behavioral control of body temperature. For example, work or exercise in hot environments can produce heat faster than peripheral mechanisms can lose it.

Classification

Mild

severe

Severity

Non-exertional

Exertional

Etiology

Patients at risk for heat illness :

Athletes exercising strenuously in hot climates

Elderly patients

Infants and small children

Patients with cardiac disease or those taking beta-blockers

Patients prone to higher endogenous heat production

Poor physical fitness

Obesity

Dehydration

Patients taking medications that inhibit sweat production

or increase heat production (eg, anticholinergics,

antidepressants, antihistamines, neuroleptics, zonisamide,

sympathomimetics, lithium, alpha- and beta-blockers)

Patients at risk for heat illness :

Causes of Hyperthermia Syndromes

Heat Stroke Exertional: Exercise in higher than normal heat and/or humidity Nonexertional: Anticholinergics, including antihistamines; antiparkinsonian drugs; diuretics;

phenothiazines Drug-Induced Hyperthermia Amphetamines, cocaine, phencyclidine (PCP), methylenedioxymethamphetamine (MDMA;

"ecstasy"), lysergic acid diethylamide (LSD), salicylates, lithium, anticholinergics, sympathomimetics

Neuroleptic Malignant Syndrome Phenothiazines; butyrophenones, including haloperidol and bromperidol; fluoxetine; loxapine;

tricyclic dibenzodiazepines; metoclopramide; domperidone; thiothixene; molindone; withdrawal of dopaminergic agents

Serotonin Syndrome Selective serotonin reuptake inhibitors (SSRIs), monoamine oxidase inhibitors (MAOIs),

tricyclic antidepressants Malignant Hyperthermia Inhalational anesthetics, succinylcholine Endocrinopathy Thyrotoxicosis, pheochromocytoma Central Nervous System Damage Cerebral hemorrhage, status epilepticus, hypothalamic injury

Clinical findings

Symptoms of heat exhaustion include the following: Normal to slightly elevated core temperature

Fatigue or malaise

Orthostatic hypotension, tachycardia

Clinical signs of dehydration

Nausea, vomiting, diarrhea

Intact mental status

Responsive to cool environment, fluid and electrolyte replacement

Elevated core temperature, usually greater than 40.5°C

Vague prodrome of weakness, nausea, vomiting, headache

CNS symptoms including confusion, ataxia, coma, seizures, delirium

Hot, dry skin

Hyperdynamic cardiovascular systems (high central venous pressure [CVP], low systemic vascular resistance [SVR], tachycardia)

Elevation of hepatic transaminases, usually in the tens of thousands range

Coagulopathy

Rhabdomyolysis and renal failure

Clinical findings

Treatment

Depends on severity

It’s an emergency condition

The first goal, is cooling the patient

Treatment

Treatment

cooling

Non invasive

invasive

Non invasive

Evaporative cooling

Ice water immersion

Whole-body ice packing

Strategic ice packing

Invasive

Peritoneal lavage

Gastric lavage

Prevention

تعطيلات تابستاني است و تصميم مي گيريد روز را در يك پارك تفريحي بگذرانيد .عصرگاه تصميم مي گيريد كه براي استراحت . است روز بسيار گرم و مرطوبي

همين كه روي صندلي مي نشينيد،پيرمردي . يكي از نمايش هاي ويژه را تماشا كنيدهنگامي كه به او مي . در جلوي شما از صندلي خود به روي زمين سقوط مي كند

. را بدون ايستادن دور پارك راه رفته است رسيد، همسرش مي گويد كه تمام روز چه بايد بكنيد؟. پوست صورت او داغ و خشك است و پاسخي هم نمي دهد

سرمازدگی

Definition

A core temperature below 35ºC .

Mild hypothermia – Core temperature 32 to 35ºC

Moderate hypothermia – Core temperature 28 to 32ºC

Severe hypothermia – Core temperature below 28ºC

staging

Mild (HT I) – Normal mental status with shivering. Estimated core temperature 32 to 35°C

Moderate (HT II) – Altered mental status without shivering. Estimated core temperature 28 to 32°C

Severe (HT III) – Unconscious. Estimated core temperature 24 to 28°C

Severe (HT IV) – Apparent death. Core temperature 13.7 to 24°C (resuscitation may be possible)

Death (HT V) – Death due to irreversible hypothermia (resuscitation not possible)

Pathophysiology

Body temperature reflects the balance between heat production and heat loss. Heat is generated by cellular metabolism (most prominently in the heart and liver) and lost by the skin and lungs via the following processes :

Evaporation – Vaporization of water through both insensible losses and sweat

Radiation – Emission of infrared electromagnetic energy Conduction – Direct transfer of heat to an adjacent, cooler object Convection – Direct transfer of heat to convective currents of air or

water

convective heat loss to cold air and conductive heat loss to water are the most common mechanisms of accidental hypothermia

Pathophysiology

The hypothalamus receives input from central and peripheral thermal receptors.

In response to a cold stress, the hypothalamus attempts to stimulate heat production through shivering and increased thyroid, catecholamine, and adrenal activity.

Sympathetically mediated vasoconstriction minimizes heat loss by reducing blood flow to peripheral tissues, where cooling is greatest Peripheral blood vessels also vasoconstrict in direct response to cold.

Pathophysiology

Cooling decreases tissue metabolism and inhibits neural activity. During the initial phase of cooling, shivering in response to skin cooling produces heat and increases metabolism, ventilation, and cardiac output.

Neurologic function begins declining even above a core temperature of 35°C. Once the core temperature reaches 32°C, metabolism, ventilation, and cardiac output begin to decline and shivering becomes less effective until it finally ceases as core temperature continues to drop.

mild hypothermia

Patients with mild hypothermia demonstrate tachypnea, tachycardia, initial hyperventilation, ataxia, dysarthria, impaired judgment, shivering, and so-called "cold diuresis."

Moderate hypothermia

Moderate hypothermia is characterized by proportionate reductions in pulse rate and cardiac output, hypoventilation, central nervous system depression, hyporeflexia, decreased renal blood flow, and loss of shivering. Paradoxical undressing may be observed. Atrial fibrillation, junctional bradycardia, and other arrhythmias can occur.

Severe hypothermia

Severe hypothermia can lead to pulmonary edema, oliguria, areflexia, coma, hypotension, bradycardia, ventricular arrhythmias (including ventricular fibrillation), and asystole

Assessment

Physical examination and temperature measurement:

The hypothermic heart is very sensitive to movement. Rough handling of the patient may precipitate arrhythmias, including ventricular fibrillation. Take care to avoid jostling the patient during the physical examination or the performance of essential procedures.

The proper diagnosis and management of hypothermia depend upon the use of a low-reading thermometer to determine core temperature . Many standard thermometers only read down to a minimum of 34ºC (93ºF) and are therefore unsuitable in this situation.

Diagnosis

The diagnosis of accidental hypothermia is made based upon a history or other evidence of environmental exposure to cold and a core temperature below 35ºC

Proper diagnosis depends upon the use of a low-reading thermometer to determine the core temperature accurately.

Management

Airway

Breathing

Circulation

The management of hypothermia requires evaluation and support of the airway, breathing, and circulation; prevention of further heat loss; initiation of rewarming appropriate to the degree of hypothermia; and treatment of complications

Management

Rewarming :

Individuals should be extracted from the hypothermic environment in the horizontal position whenever possible. Even low intensity use of peripheral muscles should be avoided, as muscular perfusion and consequently core temperature afterdrop is accelerated by exertion.

Rewarming should begin as soon as possible. Rewarming techniques are divided into: passive external rewarming

active external rewarming

active internal core rewarming

The degree of hypothermia determines the techniques implemented: mild hypothermia is treated with passive external rewarming; moderate and refractory mild hypothermia are treated with active external rewarming; and severe (and some cases of refractory moderate) hypothermia is treated with active internal rewarming.

Passive external rewarming (PER)

After wet clothing is removed, the patient is covered with blankets or other types of insulation. The resulting reduction in heat loss combines with the patient's intrinsic heat production to produce rewarming. Room temperature should be maintained at approximately 28ºC ,if possible.

Active external rewarming (AER)

During active external rewarming, some combination of warm blankets, heating pads, radiant heat, warm baths, or forced warm air is applied directly to the patient's skin.

These methods are indicated for moderate to severe hypothermia (<32ºC) and for patients with mild hypothermia who are unstable, lack physiologic reserve, or fail to respond to passive external rewarming.

Active internal rewarming (AIR)

Active internal rewarming (also called active core rewarming) is the most aggressive strategy.

It can be used alone or combined with active external rewarming (AER) in patients with severe hypothermia (<28ºC) or patients with moderate hypothermia who fail to respond to less aggressive measures.

In addition to IV administration of warmed crystalloid (40 to 42ºC), effective techniques include irrigation of the peritoneum or the thorax (via the pleural space) with warmed isotonic crystalloid, and extracorporeal blood rewarming.

برق گرفتگی

Introduction

Electricity is defined as the flow of electrons between points of high concentration to points of lower concentration (or potential).

The electrical current is the volume (or actual number) of electrons that flow between these points per second, measured in amperes.

In an alternating current (AC), the direction of flow of electrons changes on a cyclical basis. Standard household current is AC alternating at 60 cycles per second.

With direct current (DC), the direction of flow remains constant. DC current is found in batteries, railway tracks, automobile electrical systems, and lightning.

DC current tends to cause a single muscle spasm that throws the victim from the source. This results in a shorter duration of exposure, but a higher likelihood of associated trauma.

AC repetitively stimulates muscle contraction. Often, the site of exposure is at the hand, and because the flexors of the arm are stronger than the extensors, the victim may actually grasp the source, prolonging the duration of contact and perpetuating tissue injury.

Introduction

Mechanism of injury

Injuries due to electricity occur by three mechanisms:

Direct effect of electrical current on body tissues

Conversion of electrical energy to thermal energy, resulting in deep and superficial burns

Blunt mechanical injury from lightning strike, muscle contraction, or as a complication of a fall after electrocution

Injury determination

The primary determinant of injury is the amount of current flowing through the body

The voltage

Resistance

Type of current (AC or DC)

The current pathway

Duration of contact

Organ involvement

The clinical manifestations of electrical injuries range from mild superficial skin burns to severe multi-organ dysfunction and death. Cardiac

Renal

Neurologic

Skin

Musculoskeletal

Vascular, coagulation system, and other injuries

چه بايد كرد برق را قطع كنيد و يا دوشاخه. از ايمني منطقه اطمينان حاصل كنيد تماس بگيريد و اگر اين كار ميسر نبود، با اداره برق يا اورژانس. را از پريز بيرون بكشيد

.از ايشان كمك بخواهيد مصدوم را از نظرABC بررسي كنيد . اگر مصدوم افتاد، او را از نظر آسيب ستون فقرات و مهر ه ها بررسي كنيد. اگر مصدوم دچار آسيب ستون فقرات و مهره ها نبود، با بالابردن سانتيمتر مصدوم را از نظر شوك درمان 30تا 20پاهاي مصدوم تا بدن او را بگيريد كنيد؛ با انداختن پتو يا كت روي وي جلوي از دست رفتن حرارت. برق گرفتگي و. خيلي سريع بدنبال مراقبتهاي پزشكي باشيد صدمات ناشي از آن اغلب نياز به مركز مراقبت سوختگي دارد. لباس ، كف و كمربند سوخته را جدا كنيد.

اگر يك نفر در بيرون از منزل با سيم برق تماس پيدا كند، سعي ميكنيد با يك دسته يا .ميلة چوبي او را حركت دهيد

احسان با استفاده از يك قيچي برقي كهنه كه هنوز كار ميكرد در حال هرس كردن تا اينكه او لحظه اي به نرده تكيه ابتدا كار خوب پيش ميرفت. گياهان دور باغ بود

داد، و ناگهان يك جريان قوي برق از درون بدنش رد شد و باعث شد كه او به چه بايد بكنيد؟. هنگاميكه شما مي رسيد، او را بيحركت مي يابيد. زمين بيافتد

Thanks

Classic (nonexertional) heat stroke – Classic heat stroke affects individuals (most often patients over 70 years) with underlying chronic medical conditions that impair thermoregulation, prevent removal from a hot environment, or interfere with access to hydration or attempts at cooling . These conditions include cardiovascular disease, neurologic or psychiatric disorders, obesity, anhidrosis, physical disability, extremes of age, and the use of recreational drugs, such as alcohol or cocaine, and certain prescription drugs, such as anticholinergic agents or diuretics .

Exertional heat stroke – Exertional heat stroke generally occurs in young, otherwise healthy individuals who engage in heavy exercise during periods of high ambient temperature and humidity. Typical patients are athletes and military recruits in basic training. In vitro muscle fiber testing reveals evidence of susceptibility to malignant hyperthermia in some patients who present in this fashion.

Heat stroke in association with a warm environment may be categorized as exertional or nonexertional.

Exertional heat stroke typically occurs in individuals exercising at elevated ambient temperatures and/or humidity. In a dry environment and at maximal efficiency, sweating can dissipate ~600 kcal/h, requiring the production of >1 L of sweat.

Even in healthy individuals, dehydration or the use of common medications (e.g., over-the-counter antihistamines with anticholinergic side effects) may precipitate exertional heat stroke.

Nonexertional heat stroke typically occurs in either very young or elderly individuals, particularly during heat waves. According to the Centers for Disease Control and Prevention, there were 7000 deaths attributed to heat injury in the United States from 1979 to 1997. The elderly, the bedridden, persons taking anticholinergic or antiparkinsonian drugs or diuretics, and individuals confined to poorly ventilated and non-air-conditioned environments are most susceptible.

It is important to distinguish between fever and hyperthermia since hyperthermia can be rapidly fatal and characteristically does not respond to antipyretics. In an emergency situation, however, making this distinction can be difficult. For example, in systemic sepsis, fever (hyperpyrexia) can be rapid in onset, and temperatures can exceed 40.5°C (104.9°F). Hyperthermia often is diagnosed on the basis of the events immediately preceding the elevation of core temperature—e.g., heat exposure or treatment with drugs that interfere with thermoregulation. In patients with heat stroke syndromes and in those taking drugs that block sweating, the skin is hot but dry, whereas in fever the skin can be cold as a consequence of vasoconstriction. Antipyretics do not reduce the elevated temperature in hyperthermia, whereas in fever—and even in hyperpyrexia—adequate doses of either aspirin or acetaminophen usually result in some decrease in body temperature.

A high core temperature in a patient with an appropriate history (e.g., environmental heat exposure or treatment with anticholinergic or neuroleptic drugs, tricyclic antidepressants, succinylcholine, or halothane) along with appropriate clinical findings (dry skin, hallucinations, delirium, pupil dilation, muscle rigidity, and/or elevated levels of creatine phosphokinase) suggests hyperthermia. Antipyretics are of no use in treating hyperthermia. Physical cooling with sponging, fans, cooling blankets, and even ice baths should be initiated immediately in conjunction with the administration of IV fluids and appropriate pharmacologic agents (see below). If sufficient cooling is not achieved by external means, internal cooling can be achieved by gastric or peritoneal lavage with iced saline. In extreme circumstances, hemodialysis or even cardiopulmonary bypass with cooling of blood may be performed.

Malignant hyperthermia should be treated immediately with cessation of anesthesia and IV administration of dantrolene sodium. The recommended dose of dantrolene is 1–2.5 mg/kg given intravenously every 6 h for at least 24–48 h—until oral dantrolene can be administered, if needed. Dantrolene at similar doses is indicated in the neuroleptic malignant syndrome and in drug-induced hyperthermia and may even be useful in the hyperthermia of the serotonin syndrome and thyrotoxicosis. The neuroleptic malignant syndrome also may be treated with bromocriptine, levodopa, amantadine, or nifedipine or by induction of muscle paralysis with curare and pancuronium. Tricyclic antidepressant overdose may be treated with physostigmine.