溺水 到院前處置 PREHOSPITAL CARE FOR DROWNING

2024-05-24 10:03AM
轉貼侯醫師2017-06-18的發文. 他引用的文章是這篇(侯醫師也是急診醫師)
Friday, June 16, 2017 Drowning in a Sea of Misinformation: Dry Drowning and Secondary Drowning
這篇文章的建議很簡單，無論醫療人員或是媒體，建議不要使用『乾溺』『二次溺水』或『接近溺水』這些沒有一致定義的名詞。
建議只使用：『溺水死亡』，與溺水後有輕微，中度與嚴重症狀（溺水後未死亡）。
原因是：溺水死亡就是CPR，溺水後沒有死亡，無論症狀多麼輕微，都建議就醫觀察。沒有區分其他型態的必要。



溺水 2019-05-19 編輯 from uptodate https://www.uptodate.com/contents/drowning-submersion-injuries#H5
PATHOPHYSIOLOGY 缺氧的原因可以是嗆到水, 水阻礙空氣進入. 或反射性喉頭痙孿, 造成呼吸道阻塞. hypoxemia=血中氧氣濃度降低; 低血氧。hypoxia 組織缺氧; cerebral hypoxia 腦缺氧;
Fatal and nonfatal drowning typically begins with a period of panic, loss of the normal breathing pattern, breath-holding, air hunger, and a struggle by the victim to stay above the water. Reflex inspiratory efforts eventually occur, leading to hypoxemia by means of either aspiration or reflex laryngospasm that occurs when water contacts the lower respiratory tract [2,3,33-36]. Hypoxemia in turn affects every organ system, with the major component of morbidity and mortality being related to cerebral hypoxia[21].
古老的文獻強調鹹水與淡水溺水有差異, 高張的鹽水進入肺部, 會導致血漿水分被抽進肺的組織間隙及肺泡, 導致大片肺水腫, 引起血清滲透壓上升. 淡水溺水會產生相反的結果, 低張的水會很快進入肺組織, 進入血管, 導致體液過多, 血清電解質被稀釋, 但之後的研究發現, 這兩種差異與病患是否到院時已經死亡比較有關係, 到院仍有呼吸心跳的患者, 差異沒那麼大. 在體液容積改變之前, 身體必須要嗆入每公斤 11cc 的水, 在電解質出現變化之前, 身體必須嗆入每公斤22cc的水, 對於非致死性溺水的患者, 嗆入每公斤超過 3-4 cc 的水是相當罕見的, 所以以現在的觀點看起來, 淡水或鹹水溺水似乎不是那麼重要, 兩種溺水都會造成肺功能下降, 通氣-灌流不匹配, intrapulmonary shunt 是指, 血流流經沒有氣體進出的肺組織, 形成無效血流, 醫學上稱為shunt. 這些最後導致血中氧氣降低 (低血氧 hypoxemia) 造成很多器官功能不良, 水溫以及水中的汙染物對於病患的預後也有影響.
(補充. aspiration 醫學上翻譯成吸入性. 例如酒醉的人. 胃裡面吐出來的東西, 進入肺部造成發炎, 稱 aspiration pneumonia. 吸入性肺炎; 醫療上的行為, 也會用到aspiration. 例如用細針, 戳入疑似異常的組織內, 將抽出的細胞送病理檢查, 也稱為aspiration. 如 fine needle aspiration. 所以aspiration 又有抽出的意思. )
The literature formerly emphasized the distinction between salt water and fresh water drowning [37]. It was believed that the hypertonicity of salt water caused plasma to be drawn into the pulmonary interstitium and alveoli, leading to massive pulmonary edema and hypertonic serum. Drowning in fresh water was thought to create the opposite effect, with aspirated hypotonic fluid rapidly passing through the lungs and into the intravascular compartment, leading to volume overload and dilutional effects on serum electrolytes.
Subsequently, researchers have recognized that this distinction is more apparent among persons who are dead on arrival than among victims who are brought to the hospital alive. Aspiration of more than 11 mL/kg of body weight must occur before blood volume changes occur, and more than 22 mL/kg before electrolyte changes take place [38-40]. Because it is unusual for nonfatal drowning victims to aspirate more than 3 to 4 mL/kg, the distinction between salt water and fresh water drowning is no longer considered important [41-43]. Both types of nonfatal drowning result in decreased lung compliance, ventilation-perfusion mismatching, and intrapulmonary shunting, leading to hypoxemia that causes diffuse organ dysfunction [37]. The temperature of the water and the presence of contaminants may affect patient outcomes [3,20,33].
Prehospital care and acute interventions — 到院前處置.
沒有呼吸心跳的傷者,. 旁人立即CPR可改善預後, 但救援者要注意自身安全, 一邊CPR一邊將傷者移出水中.
Rescue and immediate resuscitation by bystanders improves the outcome of drowning victims [16,53,54]. The need for cardiopulmonary resuscitation (CPR) is determined as soon as possible without compromising the safety of the rescuer or delaying the removal of the victim from the water.
通氣, 或者說人工呼吸, 是對溺水傷者ㄧ開始最重要的治療, 一旦將傷者挪到淺水區或穩定的表面(例如水中大石頭), 沒有危險疑慮時, 應盡早開始人工呼吸, 溺水傷者與成人心跳停止的急救流程順序不同, 強調的是早一點開始人工呼吸, 而非壓胸, 給予兩口氣之後(每次一秒, 胸部有起伏代表吹氣成功, 胸部下降即可吹第二口氣). 如果傷者仍無反應, 則應開始高品質壓胸(速率100次/每分鐘, 深度 5-6 公分). 包括盡早取得AED. 根據標準CPR流程指引操作.
Ventilation is the most important initial treatment for victims of submersion injury and rescue breathing should begin as soon as the rescuer reaches shallow water or a stable surface. Note that the priorities of CPR in the drowning victim differ from those in the typical adult cardiac arrest patient, which emphasize immediate uninterrupted chest compressions. If the patient does not respond to the delivery of two rescue breaths that make the chest rise, the rescuer should immediately begin performing high-quality chest compressions. CPR, including the application of an automated external defibrillator, is then performed according to standard guidelines.
溺水患者發生頸椎受傷狀況並不常見, 除非有明顯頸椎受傷的現象或機轉, 例如跳入淺水撞擊頭部, 例行性保護頸椎會干擾呼吸道處置, 因此不建議對所有溺水傷者都這樣作. 一項針對 2244 位溺水患者的研究發現, 僅 11 位(0.5%) 發生頸椎受傷, 所有傷者均有明顯受傷徵象(signs 旁人觀察到的)及外傷機轉(例如, 潛水, 水上機動裝置事故). 對於昏迷的傷者, 臨床醫師在移除頸圈的時候則要小心評估是否可能合併頸椎損傷.
Cervical spinal cord injury is uncommon in nonfatal drowning victims, UNLESS there are clinical signs of injury or a concerning mechanism (eg, dive into shallow water). According to the AHA Guidelines for Advanced Cardiac Life Support (ACLS), routine cervical spine immobilization can interfere with essential airway management and is not recommended [7,55]. A cohort study of 2244 submersion victims reported that 11 (0.5 percent) sustained cervical spine injuries and all had obvious signs of injury and a mechanism (eg, diving, motor vehicle crash) suggestive of spinal trauma [56]. Nevertheless, it can be difficult to assess the spine of nonfatal drowning patients with an altered mental status (eg, intoxicated) and clinicians should use caution when deciding to remove spinal immobilization.
溺水傷者可能出現致命性心律不整, 這些則依據 ACLS 流程治療, 低體溫傷者合併心跳過慢或心房顫動時, 脈搏可能很微弱, 很難觸摸,
Drowning patients can present with life-threatening arrhythmias, and these are treated according to ACLS protocols. Pulses may be very weak and difficult to palpate in the hypothermic patient with sinus bradycardia or atrial fibrillation; a careful search for pulses should be performed for at least one minute before initiating chest compressions in the hypothermic patient because these arrhythmias require no immediate treatment. If the patient does not respond to the delivery of two rescue breaths that make the chest rise, the rescuer should immediately begin performing high-quality chest compressions once the absence of a pulse is established in the hypothermic patient. CPR is then performed according to standard BLS guidelines. (See "Advanced cardiac life support (ACLS) in adults" and "Pediatric advanced life support (PALS)" and "Accidental hypothermia in adults", section on 'Airway, breathing, circulation' and "Accidental hypothermia in adults", section on 'Treatment of arrhythmia'.)
The Heimlich maneuver or other postural drainage techniques to remove water from the lungs are of no proven value, and rescue breathing should not be delayed in order to perform these maneuvers [16,55,57]. High-flow supplemental oxygen should be administered to spontaneously breathing patients by facemask; apneic patients should be intubated. Attempts at rewarming hypothermic patients with a core temperature <33ºC should be initiated, either by passive or active means as available.


參考資料：http://emedicine.medscape.com/article/772753-treatment
2019-05-19 20:00 剛才發現. https://emedicine.medscape.com/article/772753-overview#a3 emedicine 內容也修改了...l跟 uptodate 差不多....


Pathophysiology
The most important contributory factors to morbidity and mortality from drowning are hypoxemia and acidosis and the multiorgan effects of these processes. Central nervous system (CNS) damage may occur because of hypoxemia sustained during the drowning episode (primary injury) or may result from arrhythmias, ongoing pulmonary injury, reperfusion injury, or multiorgan dysfunction (secondary injury), particularly with prolonged tissue hypoxia.
After initial breath holding, when the victim's airway lies below the liquid's surface, an involuntary period of laryngospasm is triggered by the presence of liquid in the oropharynx or larynx. At this time, the victim is unable to breathe in air, causing oxygen depletion and carbon dioxide retention. As the oxygen tension in blood drops further, laryngospasm releases, and the victim gasps, hyperventilates, possibly aspirating variable amounts of liquid. This leads to further hypoxemia.
Lunetta et al reviewed the autopsies of 578 individuals who had apparently drowned and found evidence of water in the lungs of 98.6% of those studied. As they noted, active ventilation while submerged is required to aspirate water, as water does not passively flow into the lungs once the victim is dead. [45]
Depending upon the degree of hypoxemia and resultant acidotic change in acid-base balance, the person may develop myocardial dysfunction and electrical instability, cardiac arrest, and CNS ischemia. [46] Asphyxia leads to relaxation of the airway, which permits the lungs to take in water in many individuals, although most patients aspirate less than 4 mL/kg of fluid.
Fluid aspiration of at least 11 mL/kg is required for alterations in blood volume to occur, and aspiration of more than 22 mL/kg is required before significant electrolyte changes develop. Ingestion of large volumes of freshwater, rather than aspiration, is the likely cause of clinically significant electrolyte disturbances, such as hyponatremia, in children after drowning.
Approximately 10-15% of individuals maintain tight laryngospasm until cardiac arrest occurs and inspiratory efforts have ceased. These victims do not aspirate any appreciable fluid (previously referred to as "dry drowning") (see the chart below).
Mechanism of hypoxia in submersion injury.
Mechanism of hypoxia in submersion injury.
In young children suddenly immersed in cold water (< 20°C), the mammalian diving reflex may occur and produce apnea, bradycardia, and vasoconstriction of nonessential vascular beds with shunting of blood to the coronary and cerebral circulation.
Pulmonary effects
The target organ of submersion injury is the lung. Aspiration of as little as 1-3 mL/kg of fluid leads to significantly impaired gas exchange. Injury to other systems is largely secondary to hypoxia and ischemic acidosis. Additional CNS insult may result from concomitant head or spinal cord injury. The period of hypoxia/hypoxemia is initially limited to the duration of hypopnea or apnea and may resolve with initial rescue efforts.
Patients with prolonged hypoxic episodes are prone to alveolar fluid aspiration resulting in vagally mediated pulmonary vasoconstriction, hypertension, and fluid-induced bronchospasm. Freshwater moves rapidly across the alveolar-capillary membrane into the microcirculation. Freshwater is considerably hypotonic relative to plasma and causes disruption of alveolar surfactant. Destruction of surfactant produces alveolar instability, atelectasis, and decreased compliance, with marked ventilation/perfusion (V/Q) mismatching. As much as 75% of blood flow may circulate through hypoventilated lungs.
Saltwater, which is hyperosmolar, increases the osmotic gradient and therefore draws fluid into the alveoli, diluting surfactant (surfactant washout). Protein-rich fluid then exudes rapidly into the alveoli and pulmonary interstitium. Compliance is reduced, the alveolar-capillary basement membrane is damaged directly, and shunting occurs. This results in rapid development of serious hypoxia.
The distinction between submersion fluid type is primarily academic and mostly connotes epidemiologic significance. Hypoxia serves as the primary insult and, with alveolar aspiration, culminates in surfactant disruption, alveolar collapse and derecruitment, intrapulmonary shunting, increased pulmonary vascular resistance, and ventilation-mismatch. These processes result in acute lung injury (ALI) and acute respiratory distress syndrome (ARDS).
Pulmonary hypertension may be exacerbated by inflammatory mediator release. In a minor percentage of patients, aspiration of vomitus, sand, silt, stagnant water, and sewage may result in occlusion of bronchi, bronchospasm, pneumonia, abscess formation, and inflammatory damage to alveolar capillary membranes.
Postobstructive pulmonary edema following laryngospasm and hypoxic neuronal injury with resultant neurogenic pulmonary edema may also occur. ARDS from altered surfactant effect and neurogenic pulmonary edema often complicate management.
Commonly, these edematous, noncompliant lungs may be further compromised by ventilator-associated lung injury (VALI). Newer modes of ventilation, including high-frequency oscillatory ventilation and airway pressure release ventilation, or an open-lung approach that limits tidal volumes to 6-8 mL/kg while using positive end-expiratory pressure (PEEP) to support optimal respiratory compliance, can help support oxygenation and ventilation with less risk of VALI than is associated with older methods of ventilation.
Pneumonia is a rare consequence of submersion injury and is more common with submersion in stagnant warm and fresh water. Uncommon pathogens, including Aeromonas, Burkholderia, and Pseudallescheria, cause a disproportionate percentage of cases of pneumonia. Because pneumonia is uncommon early in the course of treatment of submersion injuries, the use of prophylactic antimicrobial therapy has not proven to be of any benefit.
Chemical pneumonitis is a more common sequela than pneumonia, especially if the submersion occurs in a chlorinated pool or in a bucket containing a cleaning product.
Central nervous system effects
Hypoxic-ischemic brain injury is a foreboding sequelae of asphyxial cardiac arrest associated with drowning. The degree of CNS injury remains the major determinant of subsequent survival and long-term morbidity in cases of drowning. Two minutes after immersion, a child will lose consciousness. Irreversible brain damage usually occurs after 4-6 minutes. Most children who survive are discovered within 2 minutes of submersion. Most children who die are found after 10 minutes.
The areas of high risk in the brain are the metabolically active subcortical tissues and those with watershed perfusion. Global brain injury occurs in cases of hypoxemia and low-flow states resulting in energy failure, lipid peroxidation, free radical production, inflammatory processes, and release of excitotoxic neurotransmitters. Neuronal and glial functions are disrupted. Asphyxial cardiac arrest results in the development of microinfarctions as well as selective neuronal injury. [47, 48]
Primary CNS injury is initially associated with tissue hypoxia and ischemia. If the period of hypoxia and ischemia is brief or if the person is a very young child who rapidly develops core hypothermia, primary injury may be limited, and the patient may recover with minimal neurologic sequelae, even after more prolonged immersion.
In contrast, drowning that is associated with prolonged hypoxia or ischemia is likely to lead to both significant primary injury and secondary injury, especially in older patients who cannot rapidly achieve core hypothermia. Sources of secondary injury include the following:
Reperfusion
Sustained acidosis
Cerebral edema
Hyperglycemia
Release of excitatory neurotransmitters
Seizures
Hypotension
Impaired cerebral autoregulation
Although cerebral edema is a common consequence of prolonged submersion (or submersion followed by prolonged circulatory insufficiency), retrospective reviews and animal studies have not demonstrated any benefit from the use of intracranial pressure monitoring with diffuse axonal injury. However, as submersion injuries may be associated with trauma (especially to the head, neck, and trunk), focal or persistent neurologic deficit may indicate mass lesions or other injury amenable to surgical intervention.
Autonomic instability (diencephalic/hypothalamic storm) is common following severe traumatic, hypoxic, or ischemic brain injury. These patients often present with signs and symptoms of hyperstimulation of the sympathetic nervous system, including the following:
Tachycardia
Hypertension
Tachypnea
Diaphoresis
Agitation
Muscle rigidity
Autonomic instability has also been found to present as takotsubo stress-induced cardiomyopathy, with associated electrocardiographic changes, apical ballooning on echocardiogram, and elevated serum troponin levels. [49]
Seizures may be the result of acute cerebral hypoxia, but they may also be inciting events that lead to loss of consciousness and inability to protect the airway.
Cardiovascular effects
Drowning may result in an acute asphyxial cardiac arrest, which emanates from hypoxemia that precedes the development of ischemia. This scenario results from initial cessation of gas exchange followed by worsening hypoxia and eventual cardiac arrest. Hypoxemia is the overriding insult.
Hypovolemia may be due to fluid losses from increased capillary permeability. Profound hypotension may take place during and after the initial resuscitation period, especially when rewarming is accompanied by vasodilatation. It is important to remain cognizant that many patients present with hypothermia due to prolonged submersion times rather than true cold-water submersion.
Myocardial dysfunction may result from ventricular dysrhythmias, pulseless electrical activity (PEA), and asystole due to hypoxemia, hypothermia, acidosis, or electrolyte abnormalities (less common). In addition, hypoxemia may directly damage the myocardium, decreasing cardiac output.
Pulmonary hypertension may result from the release of pulmonary inflammatory mediators, increasing right ventricular afterload and thus decreasing both pulmonary perfusion and left ventricular preload. However, although cardiovascular effects may be severe, they are usually transient, unlike severe CNS injury.
Primary arrhythmias, including long-QT syndromes (particularly type I) and catecholaminergic polymorphic ventricular tachycardia (CPVT), may predispose patients to fatal arrhythmias during swimming. Sudden, severe cardiovascular collapse in otherwise healthy patients with brief, witnessed immersion may be the result of existing cardiac conduction defects and may not represent secondary effects of immersion injury. [50] Swimming may serve as an arrhythmogenic trigger and result in the diving reflex, which can lead to autonomic instability. The diving reflex is elicited by contact of the face with cold water and consists of breath-holding, bradycardia, and intense peripheral vasoconstriction. The exertion associated with swimming may additionally result in predisposition to syncopal events.
Infection
Infection in the sinuses, lungs, and CNS, as well as other less common sites, may result from unusual soil and waterborne bacteria, amebas, and fungi, including Pseudallescheria boydii and Scedosporium apiospermum,Naegleria, Balamuthia, as well as Burkholderia and Aeromonas organisms, and newly discovered human pathogens (Francisella philomiragia). [6, 51, 52, 53, 54, 55, 56, 57] These infections are usually insidious in onset, typically occurring more than 30 days after the initial submersion injury. P boydii‒complex infections are difficult to treat and are often fatal. [53, 58, 59]
Several investigators have suggested that the finding of evidence of seawater organisms, such as bioluminescent bacteria and plankton DNA, or normal inhabitants of the trachea in the bloodstream may be utilized as an additional indicator to support the conclusion of death by drowning in bodies discovered in aquatic environments. [60, 61]
Other effects
The clinical course may be complicated by multiorgan system failure resulting from prolonged hypoxia, acidosis, rhabdomyolysis, acute tubular necrosis, or the treatment modalities. Disseminated intravascular coagulation (DIC), hepatic and renal insufficiency, metabolic acidosis, and GI injuries must be considered and appropriately managed.
以上是新的內容.


底下是舊的內容~~~
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病患一旦被救起，如果已經回到安全區域，即使尚未離開水，應及早做人工呼吸，但胸部按壓可能無法做（浮力的影響）.


The victim should be removed from the water at the earliest opportunity. Rescue breathing should be performed while the individual is still in water, but chest compressions are inadequate because of buoyancy issues.


昏迷的病患，應檢查口中是否有異物和嘔吐物，用手指頭將之移除 (不需要強迫排出病患肺部積水, 若有嘔吐現象, 頭側一邊讓嘔吐物流出即可, 不要盲目掏挖口腔. )，壓肚子排水沒有用，反而可能造成病患嘔吐而嗆到，且會耽擱心肺復甦術開始時間。即使肺部有水，仍應做人工呼吸。


In the patient with an altered mental status, the airway should be checked for foreign material and vomitus. Debris visible in the oropharynx should be removed with a finger-sweep maneuver. The abdominal thrust (Heimlich) maneuver has not been shown to be effective in removing aspirated water; in addition, it delays the start of resuscitation and risks causing the patient to vomit and aspirate. In any event, ventilation is achieved even if fluid is present in the lungs.


如果病患清醒，將濕衣物脫掉避免失溫。但是對於昏迷、心跳停止病患，適當的低體溫有助於保護神經功能，避免缺氧性腦損傷，減少死亡(但仍需要更多的臨床研究來證實)。
More traditional literature proposes that prehospital care providers should begin rewarming. Wet clothing is ideally removed before the victim is wrapped in warming blankets. More recent studies have shown that therapeutic cooling after out-of-hospital ventricular fibrillation cardiac arrest is actually beneficial in patients to reduce ischemic brain injury and death. This area needs additional vigorous clinical research to determine the most effective treatment strategy in drowning victims.


病患如果在急診觀察 6-8 小時，且沒有下列任何一項症狀，可以出院(同樣情形應該適用於山上、野外的觀察時間)
- 僅有輕微溺水且病患能詳細說明發生的狀況(有些病患可能無法詳細說出自己當時的症狀)
- 沒有明顯外傷
- 神智及行為完全正常(有喝酒或服用鎮定劑的要觀察到完全清醒)
- 沒有氣管攣縮、心跳過快(一般是大於100次/每分鐘)、呼吸困難
- 沒有氧氣濃度不足的現象 (抽血或使用血氧濃度監視器)


Patient disposition depends on the history, presence of associated injuries, and degree of immersion injury. Patients can be safely discharged from the ED after 6-8 hours of observation if they meet the following criteria:
Able to relay a good history of minor immersion injury
No evidence of significant injury
No change in mental status or behavior
No evidence of bronchospasm or tachypnea/dyspnea
No evidence of inadequate oxygenation (by ABG analysis and pulse oximetry)
(上述狀況不適用於老年人以及有慢性病的患者)


溺水情況如果更嚴重一些，留在急診觀察時間要拉長
如果急診觀察期間出現氧氣濃度下降，應住院觀察
密切注意是否出現肺炎、中樞神經感染跡象。但不需要預防性先給抗生素（沒有用）


2002 年，溺水的專家共識會議建議，溺水病患如果發生昏迷、心跳停止，經急救後如果出現自發性循環（意思是心臟能自己跳動，不需要壓胸急救），中心體溫應該保持 在 32-34 度C，如果病患體溫超過 34 度C，應立即降溫，維持12-24小時(一天之後再回溫)。（不過這只是專家會議共識，沒有足夠的實驗和文獻證實）


A panel of experts was convened at the 2002 World Congress on Drowning, who made the following consensus recommendations on drowning management: "The highest priority is restoration of spontaneous circulation, subsequent to this continuous monitoring of core/and or brain (tympanic) temperatures is mandatory in the ED and intensive care unit and to the extent possible in the prehospital setting.
“Drowning victims with restoration of adequate spontaneous circulation who remain comatose should not be actively warmed to temperature values above 32-34°C. If core temperature exceeds 34°C, hypothermia should be achieved as soon as possible and sustained for 12 to 24 hours..." Evidence to support the use of any neuroresuscitative pharmacologic therapy is insufficient.
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溺水, 到院前處置
MANAGEMENT — Management of drowning victims can be divided into three phases: prehospital care, emergency department (ED) care, and inpatient care.
對於溺水傷患立即給予急救處置能改善傷患預後
在安全場合, 不用等離開水域, 立即給予傷患必要的 CPR,
對於溺水傷患, 人工呼吸是最重要的急救步驟. 傷患出水立即給予, 跟一般心跳停止病患的急救有點不同, 如果吹氣之後無反應, 胸部無起伏, 應依照標準急救步驟, 立即壓胸, 接上 AED 評估是否需要電擊
Prehospital care and acute interventions — Rescue and immediate resuscitation by bystanders improves the outcome of drowning victims [49]. The need for cardiopulmonary resuscitation (CPR) is determined as soon as possible without compromising the safety of the rescuer or delaying the removal of the victim from the water.
Ventilation is the most important initial treatment for victims of submersion injury and rescue breathing should begin as soon as the rescuer reaches shallow water or a stable surface. Note that the priorities of CPR in the drowning victim differ from those in the typical adult cardiac arrest patient, which emphasize immediate uninterrupted chest compressions. If the patient does not respond to the delivery of two rescue breaths that make the chest rise, the rescuer should immediately begin performing high-quality chest compressions. CPR, including the application of an automated external defibrillator, is then performed according to standard guidelines. (See "Basic life support (BLS) in adults" and "Pediatric basic life support for healthcare providers".)
頸椎傷害不常見, 除非傷患臨床上有受傷跡象, 或高危險創傷機制才需懷疑. 不建議例行性頸椎固定, 因為可能干擾呼吸道處置.
Cervical spinal cord injury is uncommon in nonfatal drowning victims, unless there are clinical signs of injury or a concerning mechanism (eg, dive into shallow water). According to the 2010 AHA Guidelines for Advanced Cardiac Life Support (ACLS), routine cervical spine immobilization can interfere with essential airway management and is not recommended [7]. A cohort study of 2244 submersion victims reported that 11 (0.5 percent) sustained cervical spine injuries and all had obvious signs of injury and a mechanism (eg, diving, motor vehicle crash) suggestive of spinal trauma [50]. Nevertheless, it can be difficult to assess the spine of nonfatal drowning patients with an altered mental status (eg, intoxicated) and clinicians should use caution when deciding to remove spinal immobilization.
溺水傷患可能發生致命性心律不整, 在心搏過緩或心房顫動傷患, 脈搏可能很微弱不易摸到, 檢查時間需至少一分鐘, 再決定是否進行胸部按壓, 如果吹氣之後病患無反應, 或者胸部無起伏, 立即進行胸部按壓(依照BLS標準急救步驟).
Drowning patients can present with life-threatening arrhythmias, and these are treated according to ACLS protocols. Pulses may be very weak and difficult to palpate in the hypothermic patient with sinus bradycardia or atrial fibrillation; a careful search for pulses should be performed for at least one minute before initiating chest compressions in the hypothermic patient because these arrhythmias require no immediate treatment. If the patient does not respond to the delivery of two rescue breaths that make the chest rise, the rescuer should immediately begin performing high-quality chest compressions once the absence of a pulse is established in the hypothermic patient. CPR is then performed according to standard BLS guidelines. (See "Advanced cardiac life support (ACLS) in adults" and "Pediatric advanced life support (PALS)" and "Accidental hypothermia in adults", section on 'Airway, breathing, circulation'and "Accidental hypothermia in adults", section on 'Treatment of arrhythmia'.)
哈姆立克法或者姿勢性引流沒有效果, 不要因為這些急救方式耽誤人工呼吸, 能自己呼吸的病患可以用氧氣面罩給予高流量氧氣, 呼吸停止病患需要插管,. 中心體溫小於 33 度c 的病患需給予回溫.
The Heimlich maneuver or other postural drainage techniques to remove water from the lungs are of no proven value, and rescue breathing should not be delayed in order to perform these maneuvers [51]. High-flow supplemental oxygen should be administered to spontaneously breathing patients by facemask; apneic patients should be intubated. Attempts at rewarming hypothermic patients with a core temperature <33ºC should be initiated, either by passive or active means as available. (See "Accidental hypothermia in adults".)