Life-Threatening Conditions and General Interventions Diabetic Ketoacidosis DEFINITION Diabetic ketoacidosis (DKA) is a life-threatening complication in patients with untreated diabetes mellitus (chronic high blood sugar or hyperglycemia). Near complete deficiency of insulin and elevated levels of certain stress hormones combine to cause DKA. DKA is more common among Type I diabetics, but may also occur in Type II diabetics generally when physiologically stressed, such as during an infection. Patients with new, undiagnosed Type I diabetes frequently present to hospitals with DKA. DKA can also occur in a known diabetic who fails to take prescribed insulin. DKA was a major cause of death in Type I diabetics before insulin injections were available; untreated DKA has a high mortality rate. PATHOPHYSIOLOGY DKA is characterized by hyperglycemia, acidosis, and high levels of circulating ketone bodies. The pathogenesis of DKA is mainly due to acidosis. Excessive production of ketone bodies lowers the pH of the blood; a blood pH below 6.7 is incompatible with life. Onset of DKA may be fairly rapid, often within 24 hours. A key component of DKA is that there is no or very little circulating insulin so it occurs mainly (but not exclusively) in type 1 diabetes (because type 1 diabetes is characterized by a lack of insulin production in the pancreas). It is much less common in type 2 diabetes because that is closely related to cell insensitivity to insulin, not shortage or absence of insulin. Some type 2 diabetics have lost their own insulin production and must take external insulin; they have some susceptibility to DKA.
Transcript
Life-Threatening Conditions and General Interventions
Diabetic Ketoacidosis
DEFINITION
Diabetic ketoacidosis (DKA) is a life-threatening complication in patients with untreated diabetes mellitus (chronic high blood sugar or hyperglycemia). Near complete deficiency of insulin and elevated levels of certain stress hormones combine to cause DKA. DKA is more common among Type I diabetics, but may also occur in Type II diabetics generally when physiologically stressed, such as during an infection. Patients with new, undiagnosed Type I diabetes frequently present to hospitals with DKA. DKA can also occur in a known diabetic who fails to take prescribed insulin. DKA was a major cause of death in Type I diabetics before insulin injections were available; untreated DKA has a high mortality rate.
PATHOPHYSIOLOGY
DKA is characterized by hyperglycemia, acidosis, and high levels of circulating ketone bodies. The pathogenesis of DKA is mainly due to acidosis. Excessive production of ketone bodies lowers the pH of the blood; a blood pH below 6.7 is incompatible with life. Onset of DKA may be fairly rapid, often within 24 hours.A key component of DKA is that there is no or very little circulating insulin so it occurs mainly (but not exclusively) in type 1 diabetes (because type 1 diabetes is characterized by a lack of insulin production in the pancreas). It is much less common in type 2 diabetes because that is closely related to cell insensitivity to insulin, not shortage or absence of insulin. Some type 2 diabetics have lost their own insulin production and must take external insulin; they have some susceptibility to DKA.
Symptoms and Signs
• Sluggish, extreme tiredness. • Extreme thirst, despite large fluid intake. • Constant urination • Fruity smell to breath, similar to nail polish remover or peardrops. • Hyperventilation, at first rapid and shallow, then progressively deeper and less rapid. • Extreme weight-loss. • Oral Thrush may be present, or/ yeast infections that fail to go away, this is because the normal fungal/flora present in oral cavity/cervix in women, the balance is upset and bacterial began to feast on the high sugar from urine output/ dry mouth from extreme thirst. • Muscle wasting. • Agitation / Irritation / Aggression / Confusion
Complications
People with diabetic ketoacidosis need close and frequent monitoring for complications. Surprisingly, the most common complications of DKA are related to the treatment:• Hypokalemia and often, potassium depletion • Cerebral edema • Hyperglycemia • Ketoacidemia• Fluid and electrolyte depletion • Aspiration • Unrecognized renal tubular necrosis • Pulmonary edema• Myocardial Infarction
Treatment
Treatment consists of hydration to lower the osmolality of the blood, replacement of lost electrolytes, insulin to force glucose and potassium into the cells, and eventually glucose simultaneously with insulin in order to correct other metabolic abnormalities, such as lowered blood potassium (hypokalemia) and elevated ketone levels. Many patients require admission to a step-down unit or an intensive care unit (ICU) so that vital signs, urine output, and blood tests can be monitored frequently. Brain edema is not rare, and so this may suggest intensive monitoring as well. In patients with severe alteration of mental status, intubation and mechanical ventilation may be required. Survival is dependent on how badly-deranged the metabolism is at presentation to a hospital, but the process is only occasionally fatal.
Hepatic encephalopathy (HE)
DEFINITION
Hepatic encephalopathy (HE), also known as Porto systemic encephalopathy or PSE, is defined as mental or neuromotor dysfunction in a patient with acute or chronic liver disease. Several forms of HE have been described the acute form of HE is often associated with fulminant hepatic failure and may rapidly progress to seizures, coma, decerebrate posturing and death. In patients with cirrhosis, acute encephalopathy is most commonly associated with a precipitating factor such as electrolyte disturbance, medications, gastrointestinal hemorrhage, or infection. Recurrent HE may occur with or without a precipitating factor and is usually easily reversible. Persistent HE is rare, and is defined as the persistence of neuropsychiatric symptoms despite aggressive medical and dietary therapy. The most frequent form of HE is not always clinically apparent: a patient with sub clinical HE has only mild cognitive deficits or subtle personality changes. Specific neuropsychological or neurophysiologic testing is required to secure the diagnosis.
PREVALENCE
By definition, all patients with fulminant hepatic failure have some degree of hepatic encephalopathy. Because there is no definitive test for HE, the prevalence in other patients is difficult to describe. Clinical findings may be apparent in as many as one third of cirrhotic patients; if rigorously tested, up to two thirds have some degree of mild or sub clinical hepatic encephalopathy.
PATHOPHYSIOLOGY
HE remains a complex clinical problem, the precise mechanism of which is unknown. The premise of most pathophysiologic theories is that ammonia accumulates in the central nervous system producing alterations of neurotransmission that affect consciousness and behavior. These "ammonia toxicity" theories have been supported by studies demonstrating increased ammonia levels in patients with both fulminant hepatic failure and chronic liver disease. The lack of strong correlation between serum ammonia levels and stage or degree of encephalopathy has been used in the argument that hyperammonemia may not be the sole factor in HE pathogenesis.
SIGNS AND SYMPTOMS
In patients with progressive HE, there is a gradual decrease in level of consciousness, intellectual capacity, and logical behavior along with development of specific neurologic deficits. Two staging systems have been described. (1) Numerous studies have employed the West Haven criteria of altered mental status in patients with HE.
DIAGNOSIS
HE is a diagnosis of exclusion. Similar neuropsychiatric symptoms are seen in a variety of metabolic disorders, toxic ingestions, or intracranial processes in certain patients, brain imaging or electroencephalography may be indicated to exclude an intracranial abnormality. Lumbar puncture with cerebrospinal fluid analysis may also be required in patients with unexplained fever, leukocytosis, or symptoms suggestive of meningeal irritation. Knowledge of the existence of acute or chronic liver disease and/or the history of HE are often helpful in heightening clinical suspicion and/or securing the diagnosis.
The main objectives in the treatment of HE are fourfold: (1) provide supportive care, (2) correct any precipitating factors, (3) reduce the nitrogen load in the gastrointestinal tract, and (4) assess the need for long-term therapy. Each of these objectives will be discussed separately here.
Standard supportive care is required for all hospitalized patients with HE. Patient safety and frequent monitoring of mental status is crucial. This may require additional personnel. In the case of comatose patients, admission to the intensive care unit and/or endotracheal intubation may be necessary. Patients with HE should also avoid prolonged periods of fasting. Although the restriction of dietary protein at the time of acute HE is often a cornerstone of therapy, protracted nitrogen restriction can lead to malnutrition. Therefore, appropriate enteral nutrition, either by mouth or nasogastric feeding tube, should be administered as soon as feasible.
KIDNEY FAILURE / END STAGE RENAL DISEASE
DEFINITION
Renal failure or kidney failure is a situation in which the kidneys fail to function adequately. It is divided in acute and chronic forms; either form may be due to a large number of other medical problems.Biochemical, it is typically detected by an elevated serum creatinine. In the science of physiology, renal failure is described as a decrease in the glomerular filtration rate. When the kidneys malfunction, problems frequently encountered are abnormal fluid levels in the body, deranged acid levels, abnormal levels of potassium, calcium, phosphate, hematuria (blood in the urine) and (in the longer term) anemia. Long-term kidney problems have significant repercussions on other diseases, such as cardiovascular disease.
ClassificationRenal failure can broadly be divided into two categories: acute renal failure and chronic kidney disease.The type of renal failure (acute vs. chronic) is determined by the trend in the serum creatinine. Other factors which may help differentiate acute and chronic kidney disease
include the presence of anemia and the kidney size on ultrasound. Long-standing, i.e. chronic, kidney disease generally leads to anemia and small kidney size.Causes Unlike acute renal failure, chronic renal failure slowly gets worse. It most often results from any disease that causes gradual loss of kidney function. It can range from mild dysfunction to severe kidney failure. The disease may lead to end-stage renal disease (ESRD).Chronic renal failure usually occurs over a number of years as the internal structures of the kidney are slowly damaged. In the early stages, there may be no symptoms. In fact, progression may be so slow that symptoms do not occur until kidney function is less than one-tenth of normal.Chronic renal failure and ESRD affect more than 2 out of 1,000 people in the United States. Diabetes and high blood pressure are the two most common causes and account for most cases. Other major causes include:• Alport syndrome • Analgesic nephropathy • Glomerulonephritis of any type (one of the most common causes) • Kidney stones and infection • Obstructive uropathy • Polycystic kidney disease • Reflux nephropathy
Symptoms
Initial symptoms may include the following:• Fatigue • Frequent hiccups • General ill feeling • Generalized itching (pruritus) • Headache • Nausea, vomiting • Unintentional weight loss
Exams and Tests There may be mild to severe high blood pressure. A neurologic examination may show polyneuropathy. Abnormal heart or lung sounds may be heard with a stethoscope.A urinalysis may show protein or other abnormalities. An abnormal urinalysis may occur 6 months to 10 or more years before symptoms appear.• Creatinine levels progressively increase. • BUN is progressively increased. • Creatinine clearance progressively decreases. • Potassium test may show elevated levels. • Arterial blood gas and blood chemistry analysis may show metabolic acidosis.Than normal, may be seen on: Signs of chronic renal failure, including both kidneys being smaller• Abdominal CT scan
• Abdominal MRI • Abdominal ultrasound • X-rays of the kidneys and abdomen
Treatment
The goal of treatment is to control symptoms, reduce complications, and slow the progression of the disease.Diseases that cause or result from chronic kidney failure must be controlled and treated as appropriate.Blood transfusions or medications such as iron and erythropoietin supplements may be needed to control anemia.Fluids may be restricted, often to an amount equal to the volume of urine produced. Restricting the amount of protein in the diet may slow the build up of wastes in the blood and control associated symptoms such as nausea and vomiting. Salt, potassium, phosphorus, and other electrolytes may be restricted.Dialysis or kidney transplant may eventually be needed.
Possible Complications
• Anemia • Cardiac tamponade • Changes in blood sugar metabolism • Congestive heart failure • Decreased functioning of white blood cells • Decreased immune response • Decreased libido, impotence • Dementia • Electrolyte abnormalities including hyperkalemia • Encephalopathy • End-stage renal disease • Fractures • Hemorrhage • High blood pressure • Increased infections • Joint disorders • Liver inflammation (hepatitis B or hepatitis C) • Liver failure • Loss of blood from the gastrointestinal tract • Menstrual irregularities,mscarriage, infertility • Nerve damage • Pericarditis • Peripheral neuropathy • Platelet dysfunction • Ulcers • Seizures
• Skin dryness, itching /scratching with resultant skin infection • Weakening of the bones
Prevention
Treatment of the underlying disorders may help prevent or delay development of chronic renal failure. Diabetics should control blood sugar and blood pressure closely and should refrain from smoking.
Respiratory Distress Syndrome
Adult respiratory distress syndrome (ARDS) is a diffuse pulmonary parenchymal injury associated with noncardiogenic pulmonary edema and resulting in severe respiratory distress and hypoxemic respiratory failure.
The pathologic hallmark is diffuse alveolar damage (DAD), but lung tissue rarely is available for a pathologic diagnosis.
Pathophysiology
DAD results in loss of the integrity of the alveolar-capillary barrier, transudation of protein-rich fluid across the barrier, pulmonary edema, and hypoxemia from intrapulmonary shunting. ARDS has a diversity of predisposing conditions, including direct pulmonary injury (eg, pulmonary infection or aspiration) and indirect injury (eg, sepsis, pancreatitis, multiple trauma). Frequently, ARDS develops in association with other organ dysfunction, in which case it is part of the multiple organ dysfunction syndrome (MODS).
The exact mechanism by which the predisposing condition results in DAD is not known fully, but most likely it is mediated, at least in part, by reactive oxygen radicals and proteolytic enzymes from neutrophils. Other mechanisms mediated by cytokines, complement, or endotoxin also may be involved.
The following 3 phases in the pathogenesis of ARDS have been described: Exudative phase is the initial phase, with injury to the endothelium and
epithelium, inflammation, and fluid exudation. Fibroproliferative phase follows the exudative phase and is characterized by the
influx and proliferation of fibroblasts and other cellular elements. In this phase, injury may begin to resolve or become persistent.
In those who recover, the fibrosis phase of healing is marked by resolution of inflammation and development of varying degrees of pulmonary fibrosis.
Clinical Manifestations:
Findings on physical examination are not specific for ARDS and can be found in pulmonary edema of any cause.
• Labored breathing and tachypnea (almost universally present) • Cyanosis and moist skin • Tachycardia • Hyperventilation • Scattered crackles • Increased work of breathing • Agitation • Lethargy followed by obtundation
Causes
• Many conditions have been found to precipitate ARDS. In some cases a predisposing condition cannot be identified. The following is a partial list of the most common predisposing conditions: •o Infection - Pneumonia of any etiology (especially viral) and systemic sepsis (especially gram negative) o Shock - Any type, particularly septic and traumatic shock o Aspiration - Gastric contents, near drowning, and toxic inhalation o Trauma - Pulmonary contusion, fat embolization, and multiple trauma o Other - Systemic inflammatory response syndrome, pancreatitis, postcardiopulmonary bypass, massive blood transfusion, drug ingestion (eg, heroin, methadone, barbiturates, salicylates)Imaging Studies• The chest radiograph reveals characteristic diffuse alveolar-interstitial infiltrates in all lung fields. •o In early cases, the radiographic findings may not be fully developed. o Additional localized pulmonary findings may be present if the predisposing condition involves a pulmonary process. • Chest CT may be helpful in advanced cases but is not necessary for diagnosis. • Echocardiography may be helpful to exclude a cardiogenic etiology for pulmonary edema.
Procedures
• Sputum should be collected for Gram stain and cultures (eg, bacterial, fungal, viral) if a pulmonary infection is present. These are best obtained from the lower respiratory tract shortly after endotracheal (ET) intubation. • Bronchoscopy with bronchoalveolar lavage may be helpful to identify occult pulmonary infection but is usually performed in the ICU. • A pulmonary artery catheter may be helpful to exclude cardiogenic causes but usually is placed in the ICU.
Medications:
As of yet, no medication has been shown to affect the pulmonary inflammatory process of ARDS directly. Late cases with a persistent fibroproliferative phase may respond to steroids, but these cases are not seen in the ED. Administer antibiotics following appropriate cultures in cases of pulmonary or extrapulmonary infection leading to ARDS. The mainstays of therapy are cardiopulmonary support and treatment/eradication of the underlying or predisposing conditions. Cardiovascular instability despite fluid administration is managed with catecholamines, such as dopamine and/or dobutamine.
ASTHMA
Description
Asthma is a chronic inflammatory disease of the airways. Asthma commonly is caused by physical and chemical irritants such as foods, pollens, dust mites, cockroaches, smoke, animal dander, temperature changes, respiratory infection, activity and stress. The allergic reaction in the airways can cause an immediate reaction, with obstruction occurring, and it can precipitate a late bronchial obstructive reaction several hours after the initial exposure. A common symptom is coughing in the absence of respiratory infection, especially at night.
Status Asthmaticus
a. Child displays respiratory distress despite vigorous treatment measures.
b. Status asthmaticus is a medical emergency that can result in respiratory failure and death if left untreated.
Assessment
Client has episodes of wheezing, breathlessness, dyspnea, chest tightness and cough, particularly at night and/or in the early morning.
Client has itching localized at the front of the neck or over the upper part of the back.
Exacerbations are episodes of progressively worsening shortness of breath, cough, wheezing, chest tightness, decreases in expiratory airflow because of bronchospasm, mucosal edema, and mucus plugging; air is trapped behind occluded or narrow airways, and hypoxemia can occur.
Asthmatic Episode
a. The episode begins with irritability, restlessness, headache, feeling tired, or chest tightness.
b. Respiratory symptoms include a hacking, irritable, nonproductive cough caused by bronchial edema.
c. Accumulated secretions stimulate the cough, and the cough becomes rattling and productive of frothy, clear, gelatinous sputum.
d. Child mat be pale or flushed, and the lips may have a deep, dark red color that may progress to cyanosis observed in the nailbeds and skin, especially around the mouth.
e. Restlessness, apprehension, and diaphoresis occur.f. Younger children assume the tripod sitting position; older
children sit upright with the shoulders in a hunched-over position, with the hands on the bed or a chair, and arms braced to facilitate the use of accessory muscles of breathing (child refuses to lie down).
g. Child speaks in short, broken phrases.h. Child experiences reactions.i. Hyperresonance or percussion of the chest is noted.j. Breath sounds are coarse and loud, with crackles and coarse
rhonchi and inspiratory and expiratory wheezing; expiration is prolonged.k. Exercise-induced bronchospasm: cough, shortness of breath,
chest pain or tightness, wheezing, and endurance problems during exercise.l. Severe spasm or obstruction: breath sounds and crackles may
become inaudible, and the cough is ineffective (represents a lack of air movement).m. Ventilatory failure and asphyxia: shortness of breath, with air
movement in the chest restricted to the point of absent breath sounds accompanied by a sudden rise in the respiratory rate.
Interventions: Acute EpisodeA. Assess airway patencyB. Administer humidified oxygen by nasal prongs or face mask
C. Administer quick-relief (rescue) medicationsD. Continuously monitor respiratory status, pulse oximetry, and color; be alert to
decreased wheezing or silent chest, which may signal the inability to move air.E. Initiate an intravenous line, and prepare to correct dehydration, acidosis, or electrolyte
imbalances.F. Prepare the child for a chest radiograph.G. Prepare to obtain samples for determining arterial blood gases and serum electrolytes.
Medications
A. Quick-relief (rescue medications): to treat symptoms and exacerbationsB. Long-term control (preventer medications): to achieve and maintain control of
inflammation C. Nebulizer, metered-dose inhaler or peak expiratory flow meters.
There devices deliver many of medications used to treat asthma. If the child has difficulty using the metered0dose inhaler, medication can be
administered by nebulization (medication is mixed with saline and then nebulized with compressed air by a machine).
D. Chest Physiotherapy Chest physiotherapy includes breathing exercises and physical training. Chest physiotherapy is not recommended during an acute exacerbation.
E. Allergen Control Prevention and reduction of exposure to airborne and environmental allergens. Skin testing to identify allergens; immunotherapy (hyposensitization) is not
recommended for allergens that can be eliminated effectively.
F. Home Care Measures Instruct the client in measures to eliminate allergens. Avoid extremes of environmental temperature; in cold temperatures, instruct
the child to breathe through the nose, not the mouth, and to cover the nose and mouth with a scarf.
Avoid exposure to individuals with a viral respiratory infection. Instruct the child in how to recognize early symptoms of an asthma attack. Instruct the child in the administration of medications of an asthma attack. Instruct the child in the use of nebulizer, metered-dose inhaler, or peak
expiratory flow meter. Instruct the child about the importance of home monitoring of peak expiratory
flow rate; decrease in rate may indicate impending infection or exacerbation. Instruct the child in the cleaning of devices used for inhaled medications (oral
candidiasis can occur with the use of aerosolized steroids). Encourage adequate rest, sleep, and a well-balanced diet. Instruct the child in the importance of adequate fluid intake to liquefy
secretions. Assist in developing an exercise program. Instruct the child in the procedure for respiratory treatments and exercises as
prescribed. Encourage the child to cough effectively. Encourage the parents to keep immunizations up to date; annual influenza
vaccinations are recommended. Inform other health care providers and school personnel of the asthma
condition. Allow the child to take control of self-care measures based on age
appropriateness.
PULMONARY EMBOLISM
A. Description
1. Pulmonary embolism occurs when a thrombus that forms in a deep vein detaches and travels to the right side of the heart and then lodges in a branch of the pulmonary artery.
2. Clients prone to pulmonary embolism are those at risk for deep vein thrombosis, including those with prolonged immobilization, surgery,
obesity, pregnancy, congestive heart failure, advanced age, or history of thromboembolism.
3. Fat emboli can occur as complication following a fracture of a flat long bone.
4. Treatment is aimed at preventing venous status and includes range of motion exercises and early ambulation following surgery, the use of antiembolism or pneumatic compression stockings, and preventing pressure under the popliteal space.
B. Assessment
1. Blood-tinged sputum2. Chest pain3. Cough4. Cyanosis5. Distended neck veins6. Dyspnea accompanied by anginal pleuritic pain, exacerbated by
inspiration7. Hypotension8. Wheezes on auscultation9. Shallow respiration10. Tachypnea and tachycardia
C. Interventions
1. Administer oxygen as prescribed2. Position client in high Fowler’s position3. Monitor lung sounds4. Maintain bed rest and active and passive range of motion exercises as
prescribed.5. Encourage use of incentive spirometry as prescribed6. Monitor pulse oximetry7. Prepare for intubation and mechanical ventilation for severe hypoxemia8. Administer anticoagulation therapy intravenously with heparin sodium
(bolus), followed by continuous infusion during the acute phase.9. Administer warfarin (Coumadin) orally, as prescribed, when heparin
infusion is discontinued.10. Monitor prothrombin time and partial thromboplastin time closely.11. Prepare the client the embolectomy, vein ligation, or insertion of an
umbrella filter, as prescribed.
PNEUMOTHORAX
Occurs when the parietal or visceral pleura is breached and the pleural space is exposed to positive atmospheric pressure.
Normally the pressure in the pleural space is negative or subatmospheric; this negative pressure is required to maintain lung inflation.When either pleura is breached, air enters the pleural space, and the lung or a portion of it collapses.
Types
Types of pneumothorax include simple, traumatic, and tension pneumothorax.
SIMPLE PNEUMOTHORAX
A simple, or spontaneous, pneumothorax occurs when air enters the pleural space through a breach of either the parietal or visceral pleura.Most commonly this occurs as air enters the pleural space through the rupture of a bleb or a bronchopleural fistula.A spontaneous pneumothorax may occur in an apparently healthy person in the absence of trauma due to rupture of an air-filled bleb, or blister, on the surface of the lung, allowing air from the airways to enter the pleural cavity.It may be associated with diffuse interstitial lung disease and sever emphysema.
TRAUMATIC PNEUMOTHORAX
Occurs when air escapes from a laceration in the lung itself and enters the pleural space or enters the pleural space through a wound in the chest wall.It may result from blunt trauma (eg, rib fractures), penetrating chest or abdominal trauma (eg, stab wounds or gun shot wounds), or diaphragmatic tears.May occur during invasive thoracic procedures (ie, thoracentesis, transbronchial lung biopsy, insertion of a subclavian line) in which the pleura is inadvertently punctured, or with barotraumas from mechanical ventilation.
TENSION PNEUMOTHORAX
Occurs when air is drawn into the pleural space from a lacerated lung or through a small opening or wound in the chest wall.It may be a complication of other types of pneumothorax.In contrast to open pneumothorax, the air that enters the chest cavity with each inspiration is trapped; it cannot be expelled during expiration through the air passages or the opening in the chest wall.In effect, a one way valve or ball valve mechanism occurs where air enters the pleural space but cannot escape.With each breath, tension (positive pressure) is increased within the affected pleural space.
This cause the lung to collapse and the heart, the great vessels, and the trachea to shift toward the unaffected side of the chest (mediastinal shift).Both respiration and circulatory function are compromised because of the increased intrathoracic pressure, which decreases venous return to the heart, causing decreased cardiac output and impairment of peripheral circulation.In extreme cases, the pulse may be undetectable—this is known as pulseless electrical activity.
NURSING ALERT!
Relief of tension pneumothorax is considered an emergency measure.
Assessment findings
1. Sudden sharp pain in the chest, dyspnea, diminished or absent breath sounds on affected side, tracheal shift to the opposite side (tension pneumothorax accompanied by mediastinal shift)2. Weak, rapid pulse; anxiety; diaphoresis3. Diagnostic tests
a. Chest x-ray reveals area and degree of pneumothoraxb. pCO2 elevatedc. pH decreased
Implementation
- Apply a dressing over an open chest wound- Administer oxygen as prescribed- Position the client in high fowler’s position- Prepare for chest tube placement- Monitor chest tube drainage system
Nursing interventions
1. Provide nursing care for the client with an endotracheal tube: suction secretions, vomitus, blood from nose, mouth, throat, or via endotracheal tube; monitor mechanical ventilation.2. Restore/promote adequate respiratory function.
a. Assist with thoracentesis and provide appropriate nursing care. b. Assist with insertion of a chest tube to water- seal drainage and provide appropriate nursing care.c. Continuously evaluate respiratory patterns and report any changes.
3. Provide relief/control of pain.a. Administer narcotics/analgesics/sedatives as ordered and monitor effects.b. Position client in high-Fowler’s position.
POISONING
A poison is any substance that when ingested, inhaled, absorbed, applied to the skin, or produced within the body in relatively small amounts of injuries in the body by its chemical action.Poisoning from inhalation and ingestion of toxic materials, both intentional and unintentional, constitutes a major health hazard and an emergency situation.
Emergency treatment is initiated with the following goals:
To remove or inactivate the poison before it is absorbedTo provide supportive care in maintaining vital organ systemTo administer a specific antidote to neutralize a specific poisonTo implement treatment that hastens the elimination of the absorbed poison
INGESTED (SWALLOWED) POISONS
may be corrosiveCorrosive poisons include alkaline and acid agents that can cause tissue destruction after coming in contact with mucous membranes
Alkaline products:
Lye Drain cleanersToilet bowl cleanersBleachNonphosphate detergentsOven cleanersButton batteries (batteries used to power watches, calculators, or cameras)
Pain or burning sensationsAny evidence of redness or burn in the mouth or throatPain on swallowing or an inability to swallowVomiting or droolingAge and weight of the patient
Pertinent health history
NURSING ALERT!
The area poison control center should be called if an unknown toxic agent has been taken or if it is necessary to identify an antidote for a known toxic agent.
The following gastric emptying procedures may be used as prescribed:
Syrup of ipecac to induce vomiting in the alert patient (never use with corrosive poisons)Gastric lavage for the obtunded patient. Gastric aspirate is saved and sent to the laboratory for testing (toxicology screens).Activated charcoal administration if the poison is one that is absorbed by charcoalCathartic, when appropriate
Management
Control the airway, ventilation and oxygenationManaging respiratory and its circulation in the absence of cerebral or renal damageStabilized cardiovascular and other body functionsMonitoring closely for changes in ECG, vital signs, neurologist statusInsert an indwelling urinary catheter to monitor renal functionTest for concentration of drugs or poison obtained by blood specimenDetermining what substance was taken, the amount, the time of ingestionGive water or milk to drink for dilution for patient who ingested corrosive poisonDoing gastric emptying procedure as prescribed such as: syrup of ipecac, gastric lavage, gastric aspirateAdminister the specific chemical antagonist or physiologic antagonist to reverse or diminish the effects of the toxinAdministering multiple doses of charcoal or diuresis, dialysis and hemoperfusiion
CARBON MONOXIDE POISONING
Inhaled poisons.may occur as a result of industrial or household incidents or attempted suicide.It is implicated in more deaths than any other toxin except alcohol.carbon monoxide exerts its toxic effect by binding to circulating hemoglobin and thereby reducing the oxygen-carrying capacity of the blood.
Hemoglobin absorbs carbon monoxide 200 times more readily than it absorbs oxygen.carboxyhemoglobin is called carbon monoxide-bound hemoglobin which does not transport oxygen.
Clinical manifestation
Because the CNS has critical need for oxygen, CNS symptoms predominate with carbon monoxide toxicity.A person with carbon monoxide poisoning may appear intoxicated (from cerebral hypoxia).Other signs and symptoms include headache, muscular weakness, palpitation, dizziness, and confusion, which can progress rapidly to coma.Skin color (range from pink or cherry red to cyanotic and pale is not a reliable sign.Pulse oximetry is also not valid, because the hemoglobin is well saturated.It is not saturated with oxygen, but the pulse oximeter only reads whether or not the hemoglobin is saturated; in this case, it is saturated with carbon monoxide rather than oxygen.Signs of permanent CNS damage: Psychoses, Spastic paralysis, Ataxia, Visual disturbances and Deterioration of personality.
Management
Exposure to carbon monoxide requires immediate treatment.Goals of management are to reverse cerebral and myocardial hypoxia and to hasten carbon monoxide elimination.
Whenever a patient inhales a poison, the following general measures apply:
Carry the patient to fresh air immediately; open all doors and windowsLoosen all tight clothingInitiate CPR if required; administer 100% oxygenPrevent chilling; wrap the patient in blanketsKeep the patient as quite as possibleDo not give alcohol in any form or permit the patient to smoke
SKIN CONTAMINATION POISONING (CHEMICAL BURNS)
Skin contamination injuries from exposure to chemicals with large number of offending agents diverse action and metabolic effectsthe severity of chemical burn is determined by the mechanism of action, penetrating strength and concentration and the amount and duration of exposure of the skin to the chemical
the skin should be drenched immediately with running water from a shower, hose, or faucet, except in the case of lye and white phosphorus, which should be brushed off the skin, dry.The skin should be flushed with a constant stream of water as the patient’s clothing is removed.The skin of health care personnel assisting the patient should be appropriately protected if the burn is extensive or if the agent is significantly toxic or is still present.Prolonged lavage with generous amounts of tepid water is important.In the meantime, attempts to determine the identity and characteristics of the chemical agent are necessary for future treatment.The standard burn treatment appropriate for the size and location of the wound (antimicrobial treatment, debridement, tetanus prophylaxis as prescribed) is instituted.The patient may require plastic surgery for further wound management.The patient is instructed to have the affected area reexamined at 24 and 48 hours and in 7 days because of the risk of underestimating the extent and depth of these types of injuries.
NURSING ALERT!
Water should not be applied to burns from lye or white phosphorus because of the potential for an explosion or for deepening of the burn. All evidence of these chemicals should be brushed off the patient before any flushing occurs.
Management
The skin should be drenched immediately with running water from shower, hose, or faucetWater should not be applied to burns from lye or white phosphorus because of the potential for an explosion or deepening the burnA constant stream of water should continue as the patient’s clothing is being removedProlonged lavage with generous amounts of tepid water is importantIdentify and characteristics of the chemical agent for future treatmentAntimicrobial treatmentDebridementTetanus prophylaxis as prescribedPlastic surgery if required for further wound managementReexamined the affected area at 24 and 72 hours and in 7 days due to the risk for understanding the extent and depth of these types of injuries
FOOD POISONING
is a sudden, explosive illness that may occur after ingestion of contaminated food or drinkBotulism is a serious form of food poisoning that requires continual surveillance.The key treatment is determining the source and type of food poisoning. If possible, the suspected food should be brought to the medical facility and a history obtained from the patient or family.Food, gastric contents, vomitus, serum, and feces are collected for examination.The patient’s respirations, blood pressure, level of consciousness, CVP (if indicated), and muscular activity are monitored closely.Measures are instituted to support the respiratory system.Death from respiratory paralysis can occur with botulism, fish poisoning, and other food poisonings.
Signs and Symptoms
Fluid and electrolyte imbalancesLethargyRapid pulse rateFeverOliguriaAnuriaHypotensionDeliriumHypovolemic shock
Assessment questions for Food Poisoning
How soon after eating did the symptoms occur? (Immediate onset suggests chemical, plant, or animal poisoning.)What was eaten in the previous meal? Did the food have an unusual odor or taste? (Most foods causing bacterial poisoning do not have unusual odor or taste.)Did anyone else become ill from eating the same food?Did vomiting occur? What was the appearance of the vomitus?Did diarrhea occur? (Diarrhea is usually absent with botulism and with shellfish or other fish poisoning.)Are any neurologic symptoms present? (These occur in botulism and in chemical, plant, and animal poisoning.)Does the patient have a fever? (Fever is characteristic in salmonella, ingestion of fava beans, and some fish poisoning.)What is the patient’s appearance?
Management
The key treatment is to determining the source and type of food poisoningThe suspected food should be brought to the medical facility and a history obtained from the patient or family
Food, gastric contents, vomitus, serum, and feces are collected for examinationMonitoring the patient’s respiration, blood pressure, sensorium, CVP( if indicated) and muscular activityMeasure to control nausea are also important to prevent vomitingAnti emetic medication is administered parenterally as prescribed if the patient cannot tolerate fluids or medication orallyFor mild nausea, the patient takes a sips of weak tea, carbonated drinks, or tap waterAfter 12 to 42 hours if nausea and vomiting subsides the diet gradually progress to a low-residue, blant diet
SUBSTANCE ABUSE
Is the misuse of specific substances to alter mood or behavior.Drug and alcohol abuse are two examples of substance abuse.DRUG ABUSE is the use of drugs for other than legitimate medical purposes People who abuse drugs often take a variety of drugs simultaneously (such as alcohol, barbiturates, opioids, and tranquilizers), and the combination may have additive and addictive effects.
CLINICAL MANIFESTATION
Vary with the substance used, but the underlying principles of management are essentially the same.
TREATMENT GOALS FOR A PATIENT WITH A DRUG OVERDOSE
To support the respiratory and cardiovascular functions To enhance clearance of the agentTo provide for safety of the patient and staff
ACUTE ALCOHOL INTOXICATION
Alcohol is psychotropic drug that affects mood, judgment behavior, concentration, and consciousness.Many heavy drinkers are young adults or people older than 60 years.There is a high prevalence of alcoholism among ED patients.Patients who abuse alcohol return frequency to the ED, they often frustrate and tax the patience of the health care professionals who care for them.Their management requires patience and thoughtful accurate, long-term treatment.Alcohol, or ethanol, is a multi system toxin and CNS depressant that causes drowsiness, impaired coordination, slurring of speech, sudden mood changes, aggression, belligerence, grandiosity, and uninhibited behavior.In excess, it also can cause stupor, coma, and death.
Increasingly, underage minors and college students arrive at the ED with alcohol poisoning from binge drinking.Frequently, the result is death.
Management
Treatment involves detoxification of the acute poisoning, recovery, and rehabilitation The nurse should approach the patient in a nonjudgmental manner, using a firm, consistent accepting, and reasonable attitude.Speaking in calm and slow manner is helpful because alcohol interferes with thought processes.If the patient appears intoxicated, hypoxia, hypovolemia and neurologic impairment must be ruled out before it is assumed that the patient is intoxicated.Typically, a blood specimen is obtained for analysis of the blood alcohol level.If drowsy, the patient should be allowed to sleep off the state of alcoholic intoxicationDuring this time, maintenance of a patent airway and observation for symptoms of CNS depression are essential.The patient should be undressed and kept warm with blankets.On the other hand, if the patient is noisy or belligerent, sedation may be necessary, if sedation is used, the patient should be monitored carefully for hypotension and decreased level of consciousness.Additionally, the patient is examined for alcohol withdrawal and delirium and also for injuries and organic dse, such as head injury, seizures, pulmonary infections, hypoglycemia and nutritional deficiencies, that may be masked by alcoholic intoxication.
ALCOHOL WITHRAWAL SYNDROME/ DELIIUM TREMENS
Alcohol withdrawal syndrome (AWS) is an acute toxic state that occurs as a result of sudden cessation of alcohol intake after a bout of heavy drinking or, more usually, after prolonged intake of alcohol.Severity of symptoms depends on how much alcohol was ingested and for how long.Delirium tremens may be precipitated by acute injury or infection (pneumonia, pancreatitis, hepatitis) and is the most severe form of alcohol withdrawal syndrome.
SIGNS
AnxietyUncontrollable fearTremorIrritability
AgitationInsomniaIncontinenceTalkative and preoccupiedExperience visual, tactile, olfactory, and auditory hallucinations that often are terrifying Autonomic over activity occurs and is evidenced by tachycardia, dilated pupils, and profuse perspirationUsually, all V/S are elevated in the alcohol toxic stateDelirium tremens is a life-threatening condition and carries a high mortality rate.
Management
The goals of management are to give adequate sedation and support to allow the patient to rest and recover without any danger of injury or peripheral vascular collapse.A physical examination is performed to identify pre existing or contributing illnesses or injuries,A drug history is obtained to elicit information that may facilitate adjustment of any sedative requirements.Baseline blood pressure is determined, because the patient’s subsequent treatment may depend on blood pressure changes.Usually, the patient is sedated as direct with a sufficient dosage of benzodiazepines to establish and maintain sedation, which reduce agitation prevents exhaustion, prevents seizures, and promotes sleep.The patient should be calm, able to respond, and able to maintain an airway safely on his or her own.A variety of medication and combinations of medications are used (for example chlerdiazepoxide [Librium], lorazepam and clonidine).Haloperidol or droperidol may be administered for severe acute AWS dosages are adjusted according to the patient’s symptoms and blood pressure response.The patient is placed in a calm, nonstressful environment and observed closely. The room remains lighted to minimize the potential for illusions and hallucinations.Closet and bathroom doors are closed to eliminate shadows. Some one is designated to stay with the patient as much as possible.The presence of another person has reassuring and calming effect, which helps the patient maintain contact with reality.Any visual misrepresentations (illusions) are explained to orient the patient to reality.Oral or intravenous route is used to restore fluid and electrolyte balance.Phenytoin (dilantin) or other antiseizure medications may be prescribed to prevent or control repeated withdrawal seizures.Parenteral dextrose may be prescribed if the liver glycogen level is depleted
Orange juice Gatorade or other forms of carbohydrates are given to stabilized the blood glucose level and counteract tremulousness.Supplemental vitamin therapy and high protein diet are provided as prescribed to counteract vitamin deficiency.The patient should be referred to an alcoholic treatment center for follow up care and rehabilitation.
EMERGENCY MANAGEMENT OF DRUGABUSE PATIENTS AND DRUG OVERDOSE PATIENTS
NarcoticsCocaine – intranasally ( “snorting”) inhaled into nostrils through straws.
Clinical manifestations Cocaine is a central nervous system stimulant that can increase heart rate and blood pressure and hyperpyrexia, seizures, and ventricular dysrhythmias. It produces intense euphoria then anxiety, sadness, insomnia and sexual indifference; cocaine hallucinations with delusions; psychosis with extreme paranoia and ideas of persecution and hypervigilance.
Therapeutic management.
ensure airway and ventilation.control seizures.monitor cardiovascular effectstreat for hyperthermia.if cocaine was ingested, use charcoal to treat.refer for psychiatric evaluation and treatment in an inpatient unit that eliminates access to the drug. Include drug rehabilitation counseling.
HeroinOpium or paregoricMorphine, codeine, oxycontin. Fentanyl
Clinical manifestations
Pinpoint pupils (may be dilated with sever hypoxia); decreased blood pressure. Marked respiratory depression stupor to coma fresh needle marks along course of any superficial vein; skin abscesses.
Therapeutic management
Support respiratory and cardiovascular functions.Establish an intravenous IV line; obtain blood for chemical and toxicologic analysis. Patient may be given bolus of glucose to eliminate possibility of hypoglycemia.Give narcotic antagonist (naloxone hydrochloride) as prescribed to reverse severe respiratory depression and coma.Continue to monitor level of responsiveness and respirations, pulse and blood pressure. Duration of action of naloxone hydrochloride is shorter than that of heroin; repeated dosages may be necessary.Send urine for analysisObtain an ECGDo not leave patient unattended; he or she may lapse back into coma rapidly. Clinical status may change from minute to minute. Hemodialysis may be indicated for sever drug intoxicationMonitor for pulmonary edema, Which is frequently seen in patients who abuse/ overdose on narcotics.Refer patient for psychiatric and drug rehabilitation evaluation before discharge
Actue intoxication (may mimic alcohol intoxication); respiratory depression flushed face decreased pulse rate; decreased blood pressure increasinf nystagmus depressed deep tendon reflex decreasing mental alertness difficulty in speaking poor motor coordination coma, death
Therapeutic Management
Maintain airway and provide respiratory support.Endotracheal intubation or tracheostomy is considered if there is any doubt about the adequacy of airway exchange.Check airway frequently.Perform suctioning as necessary.Support cardiovascular and respiratory functions; most deaths result from respiratory depression or shock.
Start infusion through large-gauge needle or IV catheter to support blood pressure;Coma and dehydration result in hypotension and respond to infusion of intravenous fluids with elevation of blood pressure. Sodium bicarbonate may be prescribed to alkalinize urine; it promotes excretion of barbiturates/Evacuate stomach contents or lavage as soon doses of activated charcoal may be administered.Assist with hemodialysis for severely overdose patient.Maintain neurologic and vital sign flow sheet.Patient awakening from overdose may demonstrate combative behavior.Refer for psychiatric and drug rehabilitation consultation/rehabilitation to evaluate suicide potential and drug abuse.
Provide airway support, ventilation, cardiac monitoring; insert IV line.Employ gastrointestinal GI decontamination in cases of oral overdoseKeep in calm, cool quiet environmentUse small doses of diazepam IV or haloperidol as prescribed for CNS muscular hyperactivity.Administer appropriate pharmacologic therapy as prescribed for sever hypertension and ventricular dysrhythmias. Treat seizures wit benzodiazepines. Treat sympathetic stimulation with beta blocker agents. Try to communicate with patient if delusions or hallucinations are presentPlace in a protective environment
Refer psychiatric and drug rehabilitation evaluation.
Hallucinogens or Psychedelic- type of drugsLysergic acid dietjylamide (LSD)Phencyclidine HCL (PCP_ Mescaline, PsiclocybinCannabinoids (marijuana)
Clinical manifestations
nystagmusmild hypertensionmarked confused or bordering panicincoherence hyperactivitywithdrawncombative behaviorhallucinationshypertensionflashback
Therapeutic Management
evaluate and maintain patient’s airwaydetermine by urine or serum drug screentry to communicate with and reassure the patientsedate the patient as prescribed if hyperactivity cannot be controlled; diazepam or a barbiturate may be prescribed.search for evidence for traumamanage seizuresobserve patient closelymonitor for hypertensive crisisplace patient in a protected environment
Drugs Producing sedation, intoxication or Psychological and physical dependence
endotracheal tube is inserted as a precautionassess for hypotensionevacuate stomach contents; emesis lavage; activated charcoal; catharticStart ECG monitoringadminister flumazenilrefer patient for psychiatric evaluation
Salicylate PoisoningAspirin
Clinical manifestations
restlessnesstinnitusdeafness blurring of vision hyperpneahyperpyrexia sweating epigastric pain vomitingdehydration respiratory and metabolic acidosis
Therapeutic management
Treat respiratory depression.Induce gastric emptying by lavage.Give activated charcoal to absorb aspirinSupport patient with IV infusion as prescribed to establish hydration and correct electrolyte imbalances.Enhance elimination of salicylates as directed by forces diuresis, alkalinization of urine, peritoneal dialysis, or hemodialysis, according to severity of intoxication.Monitor serum salicylate level for efficacy of treatment.Administer specific prescribed pharmacologic agent for bleeding and other problems.Refer patient for psychiatric evaluation.
Acetaminophen (present in prescription and non prescription analgesics, anti pyretics and cold remedies)
Clinical manifestations:
Lethargy to encephalopathy and deathGI upset diaphoresis Right upper quadrant pain Abnormal Liver function test, prolonged prothrombin time, increased blilirubin.Hepatomegaly.
Therapeutic Management:
Maintain airway.Obtain ecetaminophen level. Levels greater than or equal to 140 mg/kg are toxic.Laboratory studies- liver function test, prothrombin time/ partial thromboplastin time, complete blood count, blood urea nitrogen, creatinine.Administer syrup of ipecac and follow emesis with activated charcoal.Prepare for possible hemodialysis, which clears acetaminophen but does not halt liver damage.Administer N-acetylcysteine (NAC, mucomyst) as soon as possible.Refer patient for psychiatric evaluation.
Provide airway supportIf within 1 hr. after overdose, insert a nasogastric tube and instill activated charcoal with sorbitol every 4hr X3.Administer sodium bicarbonate drip to decrease dysrhythmias; the alkaline environment increases the protein binding of the metabolite.Administer vasopressors.Use only class IB antiarrhythmics, as some other types of antiarrhythmics have the same effect as TCA.
Manage seizure activity.Refer patient for psychiatric evaluation for potential suicide intent and evaluation.
