exam 4 adult health 2

hypovolemic shock

shock state resulting from decreased intravascular volume due to fluid loss

Shock

is a life-threatening condition that results from inadequate tissue perfusion. Many conditions may cause shock; irrespective of the cause, tissue hypoperfusion prevents adequate oxygen delivery to cells, leading to cell dysfunction and death.

multiple organ dysfunction syndrome (MODS)

If shock is not effectively treated, ——) which is the presence of altered function of two or more organs in an acutely ill patient such that interventions are necessary to support continued organ function may ensue, often resulting in patient death. MODS may be a complication of any form of shock but is most commonly seen in patients with sepsis.

, the BP remains within normal limits.

In the compensatory stage of shock,

STAGE 1 COMPENSATORY

Patients display the often-described “fight-or-flight” response. The body shunts blood from organs such as the skin, kidneys, and gastrointestinal (GI) tract to the brain, heart, and lungs to ensure adequate blood supply to these vital organs. As a result, the skin may be cool and pale, bowel sounds are hypoactive, and urine output decreases in response to the release of aldosterone and ADH.

FIGHT OR FLIGHT EQUALS STAGE 1 COMPENSOTORY

ALL BLOOD SUPPLY IS GONNA GO TO THE LUNGS, KIDNEYS, AND BRAIN

HYPOACTIVE BOWEL SOUNDS, LESS URINE OUTPUT, CAUSE ADH AND ADOSTERONE ARE RELEASED

LIMBS ARE GONNA BE COLD

NORMAL BP!!!!!

TACHYCARDIA

ELEVATED RESPIRATIONS

COLD SKIN

CAPILLARY REFILL NORMAL

DECREASED URINARY OUTPUT

CONFUSED/AGITATED

RESPIRATORY ALKALOSIS BECAUSE OF INCREASED RESPIRATION

VITAL SIGNS OF COMPESOROTY STAGE 1

Systolic ≤100 mm Hg

MAP ≤65 mm Hg

HR: >150👀👀

shallow respirations; crackles

PaO2 <80 mm Hg😱😱

PaCO2 >45 mm Hg

Metabolic acidosis

Mottling, petechiae

Capillary refill ≥3.5 s

Lethargy CAN NOT MOVE ANYMORE

VITAL SIGNS OF STAGE 2 PROGRESSIVE

Requires intubation and mechanical ventilation and oxygenation

Jaundice

Anuric; requires dialysis

Unconscious

Profound acidosis

VITAL SIGNS OF STAGE 3 Irreversible

fluid replacement, supplemental oxygen, and medication therapy must be initiated to maintain an adequate BP and reestablish and maintain adequate tissue perfusion

MEDICAL MANAGEMENT OF SHOCK

Early interventions include identifying the cause of shock, administering intravenous (IV) fluids and oxygen, and obtaining necessary laboratory tests to rule out and treat metabolic imbalances or infection.

serum sodium and blood glucose levels are elevated in response to the release of aldosterone and catecholamines.

GET THE BLOOD CULTURES SO ANTIBIOTICS CAN BE GIVEN!1

ALTERED LEVEL OF CONSCIOUSNESS

Normally, the pulse pressure is 30 to 40 mm Hg. Narrowing or decreased pulse pressure is an earlier indicator of shock than a drop in systolic BP

Narrowing of pulse pressure:

90 mm Hg − 70 mm Hg = 20 mm Hg

YOU BETTER IDENTIFY SHOCK EARLY LOOK AT

Respiratory rate greater than or equal to 22 breaths/min

Altered mentation

Systolic BP less than or equal to 100 mm Hg

NOTIFY THE PROVIDER OF SUSPECTED SHOCK IF THERE IS

, damage has already been occurring at the cellular and tissue levels. Therefore, the patient at risk for shock must be assessed and monitored closely before the BP falls.

By the time BP drops,

For instance, sedating agents may be given to lower metabolic demands, or the patient’s pain may be treated with opioid, nonopioid, or sedating agents (e.g., propofol, dexmedetomidine, acetaminophen) to decrease metabolic demands for oxygen

Interventions focus on decreasing tissue oxygen requirements and increasing perfusion to deliver more oxygen to the tissues.

Administration of IV fluids and medications supports BP and cardiac output, and the transfusion of packed red blood cells enhances oxygen transport.

WHAT IS GOING TO BRING THE BP BACK UP

, the mechanisms that regulate BP can no longer compensate, and the MAP falls below normal limits. Patients are clinically hypotensive; this is defined as a systolic BP of 100 mm Hg or lower, or a decrease in systolic BP of 40 mm Hg from baseline. The patient shows signs of declining mental status

This leads to failure of the heart

, resulting in a buildup of lactic acid and disruption of normal cell function.

pulmonary capillary hypoperfusion and hypoxemia.

fibrosis are common consequences, leading to acute respiratory distress syndrome (ARDS)

lack of adequate blood supply leads to arrhythmias and ischemia

chest pain and even suffer a myocardial infarction (MI).

mental status deteriorates

Acute kidney injury (AKI)

Liver enzymes (aspartate aminotransferase, alanine aminotransferase, lactate dehydrogenase) and bilirubin levels are elevated, and the patient develops jaundice.

GI ischemia can cause stress ulcers in the stomach, putting the patient at risk for GI bleeding. In the small intestine, the mucosa can become necrotic and slough off, causing bloody diarrhea.

In the second stage of shock,

cardiac troponin I [cTn-I]) increase.

IN PROGRESSSIVE STAGE OF SHOCK WHAT CARDIAC MARKER IS GOING TO BE UP

Disseminated intravascular coagulation (DIC) may occur either as a cause or as a complication of shock. In this condition, widespread clotting and bleeding occur simultaneously. Ecchymoses (bruises) and petechiae (bleeding) may appear in the skin. Coagulation times (e.g., prothrombin time, activated partial thromboplastin time) are prolonged.

WHAT HAPPENS TO CLOTTING FACTORS

Supporting the respiratory system

Optimizing intravascular volume

Supporting the pumping action of the heart

Improving the competence of the vascular system

early enteral nutritional support,

targeted hyperglycemic control with IV insulin and use of antacids,

histamine-2 (H2) blockers,

antipeptic medications to reduce the risk of GI ulceration and bleeding.

Tight glycemic control Current evidence suggests that maintaining serum glucose less than 180 mg/dL

MEDICAL MANAGEMENT OF PROGRESSIVE STAGE OF SHOCK

oral care with a toothbrush,

aseptic suction technique,

turning,

elevating the head of the bed at least 30 degrees to prevent aspiration,

implementing daily interruption of sedation as prescribed to evaluate patient readiness for extubation

assessing for acute delirium, characterized by an acute change in mental status, inattention, disorganized thinking, and altered level of consciousness

nursing MANAGEMENT OF SHOCK PREVENTING COMPLICATIONS

from temperature extremes (e.g., excessive warmth or cold, shivering), which can increase the metabolic rate and oxygen consumption and thus the cardiac workload.

To conserve the patient’s energy, the nurse should protect the patient

organ damage is so severe that the patient does not respond to treatment and cannot survive. Despite treatment, BP remains low.

Renal and liver dysfunction, compounded by the release of biochemical mediators, creates an acute metabolic acidosis.

Anaerobic metabolism contributes to a worsening lactic acidosis. Reserves of ATP are almost totally depleted, and mechanisms for storing new supplies of energy have been destroyed. Respiratory system dysfunction prevents adequate oxygenation and ventilation despite mechanical ventilatory support,

cardiovascular system is ineffective in maintaining an adequate MAP for tissue perfusion.

Multiple organ dysfunction can occur as a progression along the shock continuum or as a syndrome unto itself and is described in more detail later in this chapter.

The irreversible (or refractory) stage of shock represents the point along the shock continuum at which

. Simple comfort measures, including reassuring touches, should continue to be provided despite the patient’s nonresponsiveness to verbal stimuli

NURSING MANAGEMENT IRREVERSIBLE STAGE

Isotonic crystalloid solutions

. IV crystalloids commonly used for resuscitation in hypovolemic shock include 0.9% sodium chloride solution (normal saline) and lactated Ringer’s solution

THE BEST FLUIDS FOR HYPOVOLEMIC SHOCK ARE

ABDOMINAL COMPARTMENT SYNDROME

is a serious complication that may occur when large volumes of fluid are given. It may also occur after trauma, abdominal surgery, pancreatitis, or sepsis

fluid leaks into the intra-abdominal cavity, increasing pressure that is displaced onto surrounding vessels and organs. Venous return, preload, and cardiac output are compromised. The pressure also elevates the diaphragm, making it difficult to breathe effectively. The renal and GI systems also begin to show signs of dysfunction (e.g., decreased urine output, absent bowel sounds, intolerance of tube feeding). Abdominal compartment pressure can be measured.

Normally, it is 0 to 5 mm Hg, and a pressure of 12 mm Hg is considered to be indicative of IAH

If ACS is present, interventions that usually include surgical decompression are necessary to relieve the pressure.

WHAT HAPPENS ON ACS

albumin is the agent prescribed. Albumin is a plasma protein; an albumin solution is prepared from human plasma and is heated during production to reduce its potential to transmit disease.

The disadvantage of albumin is its high cost compared to crystalloid solutions. Resuscitation with colloid solutions has not reduced the risk of morbidity or death compared to resuscitation with crystalloid solutions; moreover, colloids can be considerably more expensive than crystalloid solutions

Typically, if colloids are used to treat tissue hypoperfusion,

cardiovascular overload, pulmonary edema, and ACS.

Lung sounds are auscultated frequently to detect signs of fluid accumulation. Adventitious lung sounds, such as crackles, may indicate pulmonary edema and ALI and ARDS.

Close monitoring of the patient during fluid replacement is necessary to identify side effects and complications. The most common and serious side effects of fluid replacement are

adventitious sounds, signs and symptoms of interstitial edema, work of breathing (i.e., increasing effort required for the patient to breathe, depth of breathing, respiratory rate), and changes in oxygen saturation.

When administering large volumes of crystalloid solutions, the nurse must monitor the lungs for

vital signs must be monitored frequently (at least every 15 minutes until stable, or more often if indicated).

When vasoactive medications are given,

central venous line, because infiltration and extravasation of some vasoactive medications can cause tissue necrosis and sloughing

Vasoactive medications should be given through a

be stopped abruptly, because this could cause severe hemodynamic instability, perpetuating the shock state.

Vasoactive medications should never

3000 calories daily

Patients in shock may require more than

Dobutamine

Dopamine

Epinephrine

Milrinone

Improve contractility, increase stroke volume, increase cardiac output

Increase oxygen demand of the heart

Inotropic Agents

Nitroglycerin

Nitroprusside

Reduce preload and afterload, reduce oxygen demand of heart

Cause hypotension

Vasodilators

Norepinephrine

Dopamine

Phenylephrine

Vasopressin

Epinephrine

Angiotensin II

Increase blood pressure by vasoconstriction

Increase afterload, thereby increasing cardiac workload; compromise perfusion to skin, kidneys, lungs, gastrointestinal tract

Vasopressor Agents

Hypovolemic shock occurs when there is a reduction in intravascular volume by 15% to 30%, which represents an approximate loss of 750 to 1500 mL of blood in a 70-kg (154-lb) person

Hypovolemic shock occurs when there is a

Trauma

Surgery

Vomiting

Diarrhea

Diuresis

Diabetic ketoacidosis

Diabetes insipidus

Hypovolemic Shock

External: Fluid Losses

Hemorrhage

Burns

Ascites

Peritonitis

Dehydration

Necrotizing pancreatitis

Internal: Fluid Shifts

there isn’t enough blood in the blood vessels (like from bleeding or dehydration). Because there’s less blood, not enough comes back to the heart. With less blood to pump, the heart can't fill up properly. This means it pumps out less blood each beat (lower stroke volume) and overall less blood each minute (lower cardiac output). When that happens, blood pressure drops, and the body’s tissues don’t get the oxygen and nutrients they need.

Hypovolemic shock starts when

stop the bleeding. This may involve applying pressure to the bleeding site or surgical interventions to stop internal bleeding.

If the patient is hemorrhaging, efforts are made to .

medications to treat diarrhea and vomiting are given while efforts are made to identify and treat the cause. In older adult patients, dehydration may be the cause of hypovolemic shock.

If the cause of the hypovolemia is diarrhea or vomiting,

rapid fluid resuscitation does not cause hypothermia.

IV fluids may need to be warmed when large volumes are given

Temperature should also be monitored closely to ensure that

sepsis as a result of inadequate tissue perfusion.

The precise mechanism by which MODS occurs remains unknown, but it is most commonly seen in patients with

lungs, and cardiovascular instability, as well as failure of the hepatic, GI, renal, immunologic, and central nervous systems,

Organ failure usually begins

dyspnea and respiratory failure that are manifested as ALI or ARDS, requiring intubation and mechanical ventilation

Typically, the lungs are the first organs to show signs of dysfunction. The patient experiences progressive

hyperglycemia (elevated blood glucose level), hyperlactic acidemia (excess lactic acid in the blood), and increased BUN, are present. The metabolic rate may be 1.5 to 2 times the basal metabolic rate. At this time, there is a severe loss of skeletal muscle mass (autocatabolism) to meet the high energy demands of the body.

Signs of a hypermetabolic state, characterized by

(e.g., elevated bilirubin and liver function tests) and renal dysfunction (e.g., elevated creatinine and anuria) are evident

After approximately 7 to 10 days, signs of hepatic dysfunction

. supporting the patient and monitoring organ perfusion until primary organ insults are halted. Providing information and support to family members is a critical role of the nurse. The health care team must address end-of-life decisions to ensure that supportive therapies are congruent with the patient’s wishes

. Primary nursing interventions for MODS

massive loss of skeletal muscle mass makes rehabilitation a long, slow process.

t. Patients who survive MODS must be informed about the goals of rehabilitation and expectations for progress toward these goals, because

neurogenic shock:

shock state resulting from loss of sympathetic tone causing relative hypovolemia

Emergency Medical Treatment and Active Labor Act (EMTALA)

every ED with a Medicare provider agreement must perform a medical screening examination on all patients arriving with an emergency medical complaint if their acute signs and symptoms could result in serious injury or death if left untreated. EDs are also required to provide treatment aimed at stabilizing each patient’s condition. If the patient must be transferred to another facility, the patient’s consent for transfer should be obtained, if possible. In addition, acceptance by the receiving facility and primary provider must be obtained, and an appropriate method of transfer

as if conscious—that is, the patient should be touched, called by name, and provided an explanation of every procedure that is performed. As the patient regains consciousness, the nurse should orient the patient by stating their name, the date, and the location. This basic information should be provided repeatedly, as needed, in a reassuring way.

The patient who is unconscious should be treated

Anxiety and Denial

During these crises, family members are encouraged to recognize and talk about their feelings of anxiety. Asking questions is encouraged. Honest answers given at the level of the family’s understanding must be provided. Although denial is an ego-defense mechanism that protects individuals from recognizing painful and disturbing aspects of reality, prolonged denial is not encouraged or supported. The family must be prepared for the reality of what has happened and what may come

Remorse and Guilt

Expressions of remorse and guilt are common, with family members accusing themselves (or each other) of negligence or minor omissions. Family members are urged to verbalize their feelings to help them cope appropriately.

Anger

Expressions of anger, common in crisis situations, are a way of handling anxiety and fear. Anger is frequently directed by the family at the patient, but it is also often expressed toward the physician, the nurse, or admitting personnel. The therapeutic approach is to allow the anger to be expressed and to assist the family members to identify their feelings of frustration.

Grief

is a complex emotional response to anticipated or actual loss. The key nursing intervention is to help family members work through their grief and to support their coping mechanisms, letting them know that it is normal and acceptable for them to cry, feel pain, and express loss. The hospital chaplain and social services staff serve as invaluable members of the team when assisting families to work through their grief (

triage

The word—-comes from the French word trier, meaning “to sort.”

, emergent

patients had the highest priority

urgent

patients had serious health problems but not immediately life-threatening ones

nonurgent

patients had episodic illnesses.

follow the ABCDE (Airway, Breathing, Circulation, Disability, Exposure) method:

•Establish a patent airway.

•Provide adequate ventilation, employing resuscitation measures when necessary. Patients who have experienced trauma must have the cervical spine protected and chest injuries assessed first, immediately after the airway is established.

•Evaluate and restore cardiac output by controlling hemorrhage, preventing and treating shock, and maintaining or restoring effective circulation. This includes the prevention and management of hypothermia. In addition, peripheral pulses are examined, and any immediate closed reductions of fractures or dislocations are performed if an extremity is pulseless.

ED staff work collaboratively and follow the

If the patient can breathe and cough spontaneously, a partial obstruction should be suspected. The patient is encouraged to cough forcefully and to persist with spontaneous coughing and breathing efforts as long as good air exchange exists. There may be some wheezing between coughs. If the patient demonstrates a weak, ineffective cough, high-pitched noise while inhaling, increased respiratory difficulty, or cyanosis, the patient should be managed as if there were complete airway obstruction.

After the obstruction is removed, rescue breathing is initiated. If the patient has no pulse, cardiac compressions are instituted. These measures provide oxygen to the brain, heart, and other vital organs until definitive medical treatment can restore and support normal heart and ventilatory activity (ENA, 2020a). See Chapter 25 for review of current CPR guidelines.

AIRWAY Management

may be as simple as repositioning the patient’s head to prevent the tongue from obstructing the pharynx. Alternatively, other maneuvers, such as the head-tilt/chin-lift maneuver, the jaw-thrust maneuver, or insertion of specialized equipment, may be needed to open the airway, remove a foreign body, or maintain the airway

Establishing an airway

nasopharyngeal airway should not be used because it could enter the brain cavity instead of the pharynx.

In the case of potential facial trauma or basal skull fracture, the

checking for equal bilateral breath sounds. Satisfactory management of ventilations may prevent hypoxia and hypercapnia. The nurse must quickly assess for absent or diminished breath sounds, open chest wounds, and difficulty delivering artificial breaths for the patient. The nurse should monitor pulse oximetry, capnography, and arterial blood gases if the patient requires airway or ventilatory assistance.

After the airway is determined to be unobstructed, the nurse must ensure that ventilation is adequate by

hypovolemia, so ventilatory assessment precedes assessment for hemorrhage. A pneumothorax (both simple and tension) or sucking (open) chest wound is managed with a chest tube and occlusion of the sucking wound; immediate relief of increasing positive intrathoracic pressure and maintenance of adequate ventilation should occur (

A tension pneumothorax can

cool, moist skin (resulting from poor peripheral perfusion), decreasing blood pressure, increasing heart rate, delayed capillary refill, and decreasing urine volum

The patient is assessed for signs and symptoms of shock:

warmer when possible, because administration of large amounts of blood that has been refrigerated has a core cooling effect that may lead to cardiac arrest and coagulopathy.

The infusion rate is determined by the severity of the blood loss and the clinical evidence of hypovolemia. Blood replacement therapy that involves transfusing several units of blood products should be given

A firm pressure dressing is applied, and the injured part is elevated to stop venous and capillary bleeding, if possible. If the injured area is an extremity, the extremity is immobilized to control blood loss.

Direct, firm pressure is applied over the bleeding area or the involved artery at a site that is proximal to the wound (see Fig. 67-3). Most bleeding can be stopped or at least controlled by application of direct pressure. Otherwise, unchecked arterial bleeding can result in death.

is labeled with the date and time it was applied. If the patient has suffered a traumatic amputation with uncontrollable hemorrhage, the tourniquet remains in place until the patient is in the operating room. Time of tourniquet application and removal should be documented. Tourniquet placement among military personnel with battle-associated trauma has demonstrated clear mortality reduction, although it occasionally has led to amputation or fasciotomy

The tourniquet

typically, packed red blood cells, plasma, and platelets are given at a rapid rate, and the patient is prepared for more definitive treatment (e.g., surgery, pharmacologic therapy).

The patient is maintained in the supine position and monitored closely until hemodynamic or circulatory parameters improve, or until they are transported to the operating room or intensive care unit.

internal hemorrhage is suspected.

Typically, the area around the wound is cleansed with normal saline solution or a polymer agent (e.g., Shur-Clens). The antibacterial agent povidone-iodine should not be allowed to get deep into the wound without thorough rinsing.

wound cleasing

the wound may be sutured (with the patient receiving a local anesthetic).

If there are no signs of suppuration (formation of purulent drainage)

persistent pain, fever or chills, bleeding, rapid swelling, foul odor, drainage, or redness surrounding the wound.

The patient is educated about signs and symptoms of infection and is instructed to contact the primary provider or clinic if there is sudden or

Trauma (

(an unintentional or intentional wound or injury inflicted on the body from a mechanism against which the body cannot protect itself) is the fourth leading cause of death in the United States. Trauma is the leading cause of death in children and in adults younger than 44 years. The incidence is increasing in adults older than 44 years. SUD is often implicated as a factor in both blunt and penetrating trauma

assumed to have a spinal cord injury until it is proven otherwise

External evidence of trauma may be sparse or absent. Patients with multiple trauma should be

•Avoid immediate re-exposure to high temperatures; hypersensitivity to high temperatures may remain for a considerable time.

•Maintain adequate fluid intake, wear loose clothing, and reduce activity in hot weather.

•Monitor fluid losses and weight loss during workout activities or exercise and replace fluids and electrolytes.

•Use a gradual approach to physical conditioning, allowing sufficient time for return to baseline temperature.

•Plan outdoor activities to avoid the hottest part of the day (between 10 AM and 2 PM).

For older patients living in urban settings with high environmental temperatures:

•The nurse directs these patients to places where air conditioning is available (e.g., shopping mall, library, church) and advises them that fans alone are not adequate to prevent heat-induced illness.

The nurse provides the following advice for the patient treated for heat-induced illness:

in older adults because their circulatory systems are unable to compensate for stress imposed by heat. Older adults have a decreased ability to perspire as well as a decreased ability to vasodilate and vasoconstrict. They have less subcutaneous tissue, a decreased thirst mechanism, and a diminished ability to concentrate urine to compensate for heat. Many older adults do not drink adequate amounts of fluid, partly because of fear of incontinence, and thus have a greater risk of heat stroke. In addition, many older adults fear being victims of crime, so even if their residence lacks air conditioning, they tend to keep windows closed despite high temperatures and humidity levels

Most heat-related deaths occur in

profound central nervous system (CNS) dysfunction (manifested by confusion, delirium, bizarre behavior, coma, seizures); elevated body temperature (40.6°C [105°F] or higher); hot, dry skin; and usually anhidrosis (absence of sweating), tachypnea, hypotension, and tachycardia.

When assessing the patient, the nurse notes the following symptoms:

high body temperatures accompanied by headaches, anxiety, syncope, profuse diaphoresis, gooseflesh, and orthostasis.

The cardinal manifestations of heat illness include muscle cramps, particularly in the shoulders, abdomen, and lower extremities; profound diaphoresis; and profound thirst

The patient with heat exhaustion, on the other hand, may exhibit similarly

This includes establishing IV access for fluid administration.

After the patient’s clothing is removed, the core (internal) temperature is reduced to 39°C (102°F) as rapidly as possible, preferably within 1 hour. One or more of the following methods may be used as prescribed (ENA, 2020a):

•Cool sheets and towels or continuous sponging with cool water

•Ice applied to the neck, groin, chest, and axillae while spraying with tepid water

•Cooling blankets

•Immersion of the patient in a cold water bath is the optimal method for cooling

Additional supportive care may include dialysis for AKI, anticonvulsant medications to control seizures, potassium for hypokalemia, and sodium bicarbonate to correct metabolic acidosis. Benzodiazepines such as diazepam may be prescribed to suppress seizure activity, while a phenothiazine such as chlorpromazine may be prescribed to suppress shivering

heat stroke management

These patients should lie supine in a cool environment. Patients with heat exhaustion may require IV fluids but may also take oral fluids, if they are tolerated. Patients with heat illness are given oral sodium supplements and oral electrolyte solutions (ENA, 2020a). Patients who have experienced a heat-induced illness should receive education to prevent another heat-related illness

Patients with heat exhaustion or heat illness may be managed less aggressively

Nonfatal drowning

is defined as survival for at least 24 hours after submersion that caused a respiratory arrest. The most common consequence is hypoxemia. Children under 5 years of age and those over the age of 85 have the highest risk of drowning

avoiding rip currents offshore; approximately 85% of shore drownings involve a rip current.

Pool drownings can be prevented by surrounding the pool with fencing, a self-latching/closing gate, and providing swimming lessons. Supervision near water is still the best prevention measure. When boating, a personal flotation device (PFD), even for swimmers, prevents drowning events. Approximately 50% of nonfatal drownings require hospital admission for management

Drowning and nonfatal drowning can be prevented by

alcohol ingestion, inability to swim, diving injuries, hypothermia, and exhaustion. The majority of drowning events occur in pools, lakes, and bathtubs.

Factors associated with drowning and nonfatal drowning include

The use of endotracheal intubation with PEEP improves oxygenation, prevents aspiration, and corrects intrapulmonary shunting and ventilation–perfusion abnormalities (caused by aspiration of water). If the patient is breathing spontaneously, supplemental oxygen may be given by mask. However, an endotracheal tube is necessary if the patient does not breathe spontaneously.

rescribed rewarming procedures (e.g., extracorporeal warming, warmed peritoneal dialysis, inhalation of warm aerosolized oxygen, torso warming) are started during resuscitation

ECG monitoring is initiated, because arrhythmias frequently occur. An indwelling urinary catheter is inserted to measure urine output.

Nasogastric intubation is used to decompress the stomach and to prevent the patient from aspirating gastric contents.

The patient is also at heightened risk for aspiration; vomiting frequently occurs in patients requiring rescue breathing and in up to 86% of patients requiring CPR

Drowining Management

edema, ecchymosis, and hemorrhagic bullae, leading to necrosis at the site of envenomation. Symptoms include lymph node tenderness, nausea, vomiting, numbness, and a metallic taste in the mouth. Without decisive treatment, these clinical manifestations may progress to include fasciculations, hypotension, paresthesias, seizures, and coma

Classic clinical signs of envenomation are

immobilizing the injured body part below the level of the heart

Initial first aid at the site of the snakebite includes having the person lie down, removing constrictive items such as rings, providing warmth, cleansing the wound, covering the wound with a light sterile dressing, and

Corticosteroids are contraindicated in the first 6 to 8 hours after the bite because they may depress antibody production and hinder the action of antivenin (antitoxin manufactured from the snake venom and used to treat snakebites).

DO NOT GIVE IN SNAKE BITE

Crotalidae polyvalent immune Fab antivenom (FabAV or CroFab).

The most readily available antivenin in the United States is

The dose depends on the type of snake and the estimated severity of the bite. Indications for antivenin depend on the progression of symptoms, including coagulopathy and systemic reaction

Serum sickness is a type of hypersensitivity response that results in fever, arthralgias, pruritus, lymphadenopathy, and proteinuria and can progress to neuropathies

If the dose exceeds 10 vials of antivenom, serum sickness will most likely occur.

the circumference of the affected part is measured.

Premedication with diphenhydramine or cimetidine may be indicated, because these antihistamines may decrease the allergic response to antivenin.

Antivenin is given as an IV infusion whenever possible, although intramuscular administration can be used.

Before administering antivenin and every 15 minutes thereafter,

is diluted in 500 to 1000 mL of normal saline solution. The infusion is started slowly, and the rate is increased after 10 minutes if there is no reaction. The total dose should be infused during the first 4 to 6 hours after the bite.

antivenin administration

feeling of fullness in the face, urticaria, pruritus, malaise, and apprehension. These symptoms may be followed by tachycardia, shortness of breath, hypotension, and shock.

, the infusion should be stopped immediately and IV diphenhydramine given.

The most common cause of allergic reaction to the antivenin is too-rapid infusion. Reactions may consist of a

first few weeks after discharge. The patient and the patient’s family members should be educated about the clinical manifestations of serum sickness (i.e., fever; rash starting on the chest and spreading to the back; arthralgia; gastrointestinal [GI] disturbances [e.g., nausea, vomiting, diarrhea, abdominal pain], and headache) and return to the ED if they occur

It is important to note that serum sickness (hypersensitivity) can occur within the

Brown recluse

bites are painless. Systemic effects such as fever and chills, nausea and vomiting, malaise, and joint pain develop within 24 to 72 hours. The site of the bite may appear reddish to purple in color within 2 to 8 hours after the bite. Necrosis occurs in the next 2 to 4 days in approximately 10% of cases. The center of the bite may become necrotic, and surgical débridement may be necessary. Wound care consists of cleansing with soap and water, and hyperbaric oxygen treatments may be helpful. Most wounds heal within 2 to 3 months

Black widow spider

bites feel like pinpricks. Systemic effects usually occur within 30 minutes—much more rapidly than with brown recluse spider bites. Signs and symptoms include abdominal rigidity, nausea and vomiting, hypertension, tachycardia, and paresthesias. Severe pain also develops within 60 minutes and increases over 1 to 2 days. Treatment involves application of ice to the site to decrease swelling and discomfort, along with elevation and assessment of tetanus immunization status. Analgesic agents and benzodiazepines may relieve muscle spasms. Cardiopulmonary monitoring is essential. Antivenin is effective for severe black widow spider bites. This antivenin is horse serum based; therefore, testing for sensitivity must be performed prior to administration

tweezers using a straight upward pull.

Removal of tick with

Rocky Mountain spotted fever, tularemia, west Nile virus, and Lyme disease.

Ticks can carry diseases such as

erythema migrans (a classic “bull’s-eye” rash) that typically can be found in the axilla, groin, or thigh area and that appears within 4 weeks after the tick bite, with a peak manifestation time of 7 days after the bite.

Classically, this rash is at least 5 cm in diameter with bright red borders.

It is accompanied by flulike signs and symptoms that may include chills, fever, myalgia, fatigue, and headache.

Without treatment, the rash subsides within 3 to 4 weeks.

However, the rash and flulike manifestations can be significantly reduced within days if prompt treatment with antibiotic agents (e.g., doxycycline) is initiated

Lyme disease has three stages. Stage I may present with