25 Medical Emergencies - Bài viết - Bệnh Học
Đọc và ngẫm: "Lễ vật lớn nhất của đời người là khoan dung. [Trích 14 điều răn của Phật] "
Chú ý: Các nội dung sai QUY ĐỊNHLuật chính tả sẽ bị XÓA
Nếu bạn đang gởi bài, hãy đọc qua bài này!


25 Medical Emergencies

Cho điểm
Medical Emergencies
Daniel Goodenberger
General Principles
Medical emergencies may not allow time for orderly information gathering and formulation of a narrow differential diagnosis before the initiation of therapy.
The first responsibility is to provide basic life support (i.e., maintenance of an intact airway, adequate ventilation, and circulation; see Chapter 8, Critical Care).
Acute Upper Airway Obstruction
General Principles
Airway obstruction in the awake patient without ventilation:
The most likely causes are a foreign body (usually food) and angioedema.
Other causes include infection or posttraumatic hematoma.
History is often unavailable.
Airway obstruction in an unconscious patient without intact ventilation:
Such a situation may be due to obstruction by the tongue, or it may be caused by a foreign body, trauma, infection, or angioedema.
A history usually is unavailable except from paramedics or relatives.
Clinical Presentation
In the conscious patient:
Manifestations may include stridor, impaired or absent phonation, sternal or suprasternal retractions, display of the universal choking sign, and respiratory distress.
Look for urticaria, angioedema, fever, or evidence of trauma.
The unconscious patient:
The patient may have labored breathing or apnea.
Suspect airway obstruction in a nonbreathing patient who is difficult to ventilate.
Physical Examination
Partial obstruction in the awake patient with adequate ventilation:
Rapidly take a history, focusing on the causes just listed.
Perform a directed physical examination, looking for airway swelling, trismus, pharyngeal obstruction, respiratory retractions, angioedema, stridor, wheezing, and grossly swollen lymph nodes and masses in the neck.
Treatment is aimed at the underlying disease process; observe the patient carefully and be prepared to intervene to maintain an airway.
Airway obstruction in an unconscious patient without intact ventilation:
Examination reveals an unresponsive patient with no air movement or paradoxical respiratory efforts.
Examine the upper airway visually for evidence of obstruction as part of the resuscitative effort.
Partial obstruction in the awake patient with adequate ventilation:
Soft tissue radiography of the neck (posteroanterior and lateral views) is less sensitive and specific than is direct examination but may be a valuable adjunct. Such radiography should be performed in the emergency department as a portable study, as the patient should not be left unattended.
Rapid computed tomography (CT) of the airway with constant attendance is an alternative approach where available.
Other Diagnostic Procedures
Partial obstruction in the awake patient with adequate ventilation:
If the patient's condition is stable, perform indirect laryngoscopy or fiberoptic nasopharyngolaryngoscopy. A careful examination is unlikely to cause acute airway obstruction in an adult.
Differential Diagnosis
Trauma to the face and neck, foreign body, infection (croup, epiglottitis, Ludwig angina, retropharyngeal abscess, and diphtheria), tumor, angioedema, laryngospasm, anaphylaxis, retained secretions, or blockage of the upper airway by the tongue (in the unconscious patient)
Therapy is directed at rapid relief of obstruction to prevent cardiopulmonary arrest and anoxic brain damage.
Airway obstruction in the awake patient without ventilation:
Perform the Heimlich maneuver (subdiaphragmatic abdominal thrust) repeatedly until the object is expelled from the airway or patient becomes unconscious (see Chapter 8, Critical Care). Up to half of patients may require a second technique (i.e., back slaps, chest thrusts) for success.1
Airway obstruction in an unconscious patient without intact ventilation:
Perform the head tilt÷chin lift maneuver if cervical spine trauma is not suspected. Perform a jaw thrust if cervical spine trauma is suspected.
If these maneuvers are effective, place an oral or nasal airway. If they are ineffective, attempt to ventilate the patient with a bag-valve-mask apparatus. If these attempts are also unsuccessful, rapidly examine the oropharynx and hypopharynx. Avoid a blind finger sweep if it is possible to examine the airway directly using a laryngoscope and McGill forceps (if necessary) to remove a foreign body.
If laryngoscopy cannot be performed immediately and a foreign body is suspected, perform the supine Heimlich maneuver (straddling the supine patient and applying repeated subdiaphragmatic thrusts). Chest thrusts may generate higher airway pressures and be successful when abdominal thrusts have failed.
Substitute chest thrusts if the patient is very obese or is in late pregnancy.
Airway obstruction in an unconscious patient without intact ventilation:
Failure of the supine Heimlich maneuver should prompt an attempt at direct laryngoscopy and endotracheal intubation.
Establish a surgical airway if the patient cannot be intubated.
If a surgeon is not immediately available, perform needle cricothyrotomy using a 12- to 14-gauge over-the-needle catheter with high-flow oxygen (15 L/min from a 50-psi wall source).
Cricothyrotomy (see Chapter 8, Critical Care) is a preferred alternative.
General Principles
Pneumothorax may occur spontaneously or as a result of trauma.
Primary spontaneous pneumothorax occurs without obvious underlying lung disease.
Secondary spontaneous pneumothorax results from underlying parenchymal lung disease, including chronic obstructive pulmonary disease, interstitial lung disease, necrotizing lung infections, Pneumocystis jiroveci pneumonia, and cystic fibrosis.
Traumatic pneumothoraces may occur as a result of penetrating or blunt chest wounds.
Iatrogenic pneumothorax occurs after thoracentesis, central line placement, transbronchial biopsy, transthoracic needle biopsy, and barotrauma from mechanical ventilation and resuscitation.
The patient typically complains of ipsilateral chest or shoulder pain, usually of abrupt onset. An occasional patient may experience dyspnea alone. Recent chest trauma or a medical procedure may suggest the diagnosis.
Clinical Presentation
Dyspnea is usually present, and the patient sometimes has a cough.
Symptoms related to an underlying pulmonary disease process may be seen or a history of recent trauma obtained.
Physical Examination
Examination of the patient with a small pneumothorax may be normal.
There may be decreased breath sounds, decreased vocal fremitus, and a more resonant percussion note.
With a larger pneumothorax or with underlying lung disease, there may be tachypnea and respiratory distress. The affected hemithorax may be noticeably larger (due to decreased elastic recoil of the collapsed lung) and relatively immobile during respiration.
If the pneumothorax is very large, and particularly if it is under tension, the patient may exhibit severe distress, diaphoresis, cyanosis, and hypotension. The patient may have signs of recent procedures or trauma.
In addition, there may be indications of underlying lung disease such as clubbing or fever.
If the pneumothorax is the result of penetrating trauma or pneumomediastinum, subcutaneous emphysema may be felt.
A chest radiograph will reveal a separation of the pleural shadow from the chest wall. A small pneumothorax is more easily seen on a film taken during expiration. Air travels to the highest point in a body cavity; thus, a pneumothorax in a supine patient may be detected as an unusually deep costophrenic sulcus and excessive lucency over the upper abdomen caused by the anterior thoracic air. This is particularly important in the critical care unit, where radiographs of the mechanically ventilated patient are often obtained with the patient supine.
Although tension pneumothorax is a clinical diagnosis, radiographic correlates include mediastinal and tracheal shift away from the pneumothorax and depression of the ipsilateral diaphragm.
Other Tests
An electrocardiogram (ECG) may reveal diminished anterior QRS amplitude and an anterior axis shift. In extreme cases, tension pneumothorax may cause electromechanical dissociation.
Treatment depends on cause, size, and degree of physiologic derangement. A small, primary, spontaneous pneumothorax without a continued pleural air leak may resolve spontaneously. Air is resorbed from the pleural space at roughly 1.5% daily, and therefore a small (~15%) pneumothorax is expected to resolve without intervention in approximately 10 days.
Confirm that the pneumothorax is not increasing in size (repeat the chest radiograph in 6 hours if there is no change in symptoms) and send the patient home if he or she is asymptomatic (apart from mild pleurisy). Obtain follow-up radiographs to confirm resolution of the pneumothorax in 7÷10 days. Air travel is proscribed during the follow-up period, as a decrease in ambient barometric pressure results in a larger pneumothorax.
If the pneumothorax is small but the patient is mildly symptomatic, far from home, or unlikely to cooperate with follow-up, admit the patient and administer high-flow oxygen; the resulting nitrogen gradient will speed resorption.
If the pneumothorax is larger than 15%÷20% or is more than mildly symptomatic, insert a small thoracostomy tube [No. 8 French (Fr.) over a needle] in the second interspace in the midclavicular line; the air can be manually aspirated with a stopcock attached to a one-way (Heimlich) valve, or, if necessary, connected to suction.2 If the bronchopleural fistula has sealed, cough or Valsalva results in re-expansion with the one-way valve. Most such patients should be hospitalized. If the pneumothorax fails to expand or if there is a continuous large air leak, arrange for insertion of a larger tube with suction.
Pleural sclerosis to prevent recurrence is recommended by some experts but in most cases is not used after a first episode unless a persistent air leak is present.
Doxycycline or a talc slurry can be used via chest tube for patients who wish to avoid surgery or who are at high surgical risk (see Pleural Effusion, in Chapter 9, Pulmonary Disease). Apical bullectomy via thoracoscopy accompanied by pleural sclerosis has a higher success rate (78%÷91% vs. 95%÷100%).2
Individuals with a secondary spontaneous pneumothorax usually are symptomatic and require lung re-expansion.
Often a bronchopleural fistula persists, and a larger thoracostomy tube and suction are required.
If no associated effusion is present, a No. 24÷28 Fr. tube is recommended; if fluid is present, choose a larger tube (No. 34÷36 Fr.). Attach the thoracostomy tube to a three-bottle suction system or the commercial equivalent (Pleur-evac, Genzyme
Biosurgery, Cambridge, MA) and apply 20 cm H2O suction. Large air leaks may require greater suction.
Consult a pulmonologist about pleural sclerosis for persistent air leak and to prevent recurrence.
Surgery may be required for persistent air leak and should be considered for high-risk patients for prevention of recurrence.
Iatrogenic pneumothorax
Iatrogenic pneumothorax generally is caused either by introducing air into the pleural space through the parietal pleura (e.g., thoracentesis, central line placement) or by allowing intrapulmonary air to escape through breach of the visceral pleura (e.g., transbronchial biopsy). Often no further air leak occurs after the initial event.
If the pneumothorax is small and the patient is minimally symptomatic, it can be managed conservatively. If the procedure that caused the pneumothorax required sedation, admit the patient, administer oxygen, and repeat the chest radiograph in 6 hours to ensure the patient's stability. If the patient is completely alert and the chest radiograph shows no change, the patient can be discharged.
If the patient is symptomatic or if the pneumothorax is too large for expectant care, a pneumothorax catheter with aspiration or a one-way valve usually is adequate and can often be removed the following day.
Iatrogenic pneumothorax due to barotrauma from mechanical ventilation almost always has a persistent air leak and should be managed with a chest tube and suction.
Tension pneumothorax
Tension pneumothorax results from continued accumulation of air in the chest that is sufficient to shift mediastinal structures and impede venous return to the heart, resulting in hypotension, abnormal gas exchange, and, ultimately, cardiovascular collapse.
It can occur as a result of barotrauma due to mechanical ventilation, a chest wound that allows ingress but not egress of air, or a rent in the visceral pleura that behaves in the same way (“ball-valve” effect).
Suspect tension pneumothorax when a patient experiences hypotension and respiratory distress on mechanical ventilation or after any procedure in which the thorax is pierced by a needle. When the clinical situation and physical examination strongly suggest this diagnosis, decompress the affected hemithorax immediately with a 14-gauge needle attached to a fluid-filled syringe. Release of air with clinical improvement confirms the diagnosis. Seal any chest wound with an occlusive dressing and arrange for placement of a thoracostomy tube.
Heat-Induced Illness
Heat cramps
Heat cramps occur in unacclimatized individuals who engage in vigorous exercise in a hot environment; no published evidence has shown unequivocally that they are a result of salt depletion and hypotonic fluid replacement.3
Cramps typically occur in large muscle groups, most often in the legs.
Diagnosis is made on examination. The patient has moist cool skin, a normal body temperature, and minimal distress.
Treatment consists of resting the patient in a cool environment and giving salt replacement.
Administer 1/2÷1 tsp salt or a 650-mg sodium chloride tablet in 500 mL water PO or use a commercially available, oral, balanced electrolyte replacement solution.
IV therapy rarely is required, but 2 L normal saline administered over several hours resolves symptoms.
Heat exhaustion
Heat exhaustion occurs in unacclimatized individuals who exercise in the heat and is partly a result of loss of salt and water.
The patient notes headache, nausea, vomiting, dizziness, weakness, irritability, and cramps. The patient is diaphoretic, demonstrates piloerection, has postural hypotension, and has normal or minimally increased core temperature.
Treatment consists of resting the patient in a cool environment, accelerating heat loss by fan evaporation, and repleting fluids with salt-containing solutions.
If the patient is not vomiting and has stable blood pressure (BP), an oral, commercial, balanced salt solution is adequate.
If the patient is vomiting or hemodynamically unstable, check electrolytes and give 1÷2 L 0.9% saline IV.
The patient should avoid exercise in a hot environment for 2÷3 additional days.
Heat syncope
Heat syncope affects unacclimatized individuals.
Exercise in a hot environment results in peripheral vasodilation and pooling of blood, with subsequent loss of consciousness. The affected individual regains consciousness promptly when supine, and the body temperature is normal. These factors separate this syndrome from heat stroke.
Treatment consists of rest in a cool environment, fluid repletion, and a more gradual approach to building exercise endurance.
Heat stroke
General Principles
Heat stroke occurs in two varieties, each with high core temperature, which causes direct thermal tissue injury. Secondary effects include acute renal failure from rhabdomyolysis. Even with rapid therapy, mortality may reach 76% for body temperatures of 41.1°C (106°F) or higher.
Classic heat stroke
Classic heat stroke occurs after several days of heat exposure.
Individuals at risk include those who are chronically ill, dehydrated, elderly, or obese; those who have chronic cardiovascular disease; those who abuse alcohol; and those who use sedatives, hypnotics, α-adrenergic antagonists, diuretics, anticholinergics, or antipsychotics.
Abuse of phencyclidine, cocaine, and amphetamines also may contribute.
Risk factors include high humidity and lack of air-conditioning.
More than 50% may have infection at presentation.4
Typically, these patients have core temperatures higher than 40.5°C (105°F) and are comatose and anhidrotic.
Exertional heat stroke
Exertional heat stroke occurs rapidly in unacclimatized and unfit individuals who exercise in conditions of high ambient temperature and humidity.
Those at risk include athletes, soldiers, and laborers, particularly if they lack access to water. Some of the risks associated with classic heat stroke may also be present, and certain congenital diseases that impair sweating may contribute. The core temperature may be lower than 40.5°C; 50% of patients are still sweating at presentation.
Individuals with exertional heat stroke are more likely than are those with classic heat stroke to have disseminated intravascular coagulation (DIC), lactic acidosis, and rhabdomyolysis.
Diagnosis is based on the history of exposure or exercise, a core temperature usually of 40.6°C (105°F) or higher, and changes in mental status ranging from confusion to delirium and coma.
Differential Diagnosis
Malignant hyperthermia after exposure to anesthetic agents
Neuroleptic malignant syndrome associated with antipsychotic drugs
It is worth noting that neuroleptic malignant syndrome and malignant hyperthermia are both accompanied by severe muscle rigidity.
Anticholinergic poisoning
Sympathomimetic toxicity (including cocaine)
Severe hyperthyroidism
Cerebral malaria
Hypothalamic dysfunction due to stroke or hemorrhage
Brain abscess
Immediate cooling is necessary.
The best method of cooling is controversial. No study has directly compared ice water application with tepid spray. However, ice water lowers body temperature twice as quickly and is the procedure chosen when exertional heat stroke is anticipated (long-distance races, military training).5,6
Wrap the patient in sheets that are continuously wetted with ice water.
If response is insufficiently rapid, submerge the patient in ice water, recognizing that this may interfere with resuscitative efforts.7
Most emergency facilities that do not care for large numbers of heat illness cases are not equipped for this treatment. In that case, mist the patient continuously with tepid water (20°÷25°C). Cool the patient with a large electric fan with maximum body surface exposure.
Ice packs at points of major heat transfer, such as the groin, axillae, and chest, may further speed cooling.
If severely elevated core temperature does not respond to these maneuvers, gastric lavage with ice water may be helpful, although this treatment is controversial.8
Cold peritoneal lavage is not more effective than evaporative cooling.
Dantrolene sodium does not appear to be effective for the treatment of heat stroke.9 However, if malignant hyperthermia due to anesthetic agent is diagnosed, give dantrolene, 2 mg/kg IV repeated q5 min as necessary for symptom relief to a total of 10 mg/kg, followed by 1÷2 mg/kg qid for 3÷4 days. Treat neuroleptic malignant syndrome with dantrolene in the same way, but add bromocriptine, 2.5÷5.0 mg PO or per gastrostomy tube q8h.
If it is necessary to treat severe hypertension, nitroprusside may be preferable, as it promotes more rapid heat loss via peripheral vasodilation.
Shivering and vasoconstriction impair cooling and should be prevented by administration of chlorpromazine, 10÷25 mg IM, or diazepam, 5÷10 mg IV.
Monitor core temperatures continuously by rectal probe. Tympanic membrane temperature measurement does not correlate well with rectal temperature and may be affected by environmental conditions.10,11 Oral temperatures are unreliable and are frequently incorrectly low.
Discontinue cooling measures when the core temperature reaches 39°C (102.2°F), which should ideally be achieved within 30 minutes. A temperature rebound may occur in 3÷6 hours and should be retreated.
For hypotension, administer crystalloids; if refractory, treat with vasopressors and monitor hemodynamics. Avoid pure α-adrenergic agents, as they cause vasoconstriction and impair cooling. Administer crystalloids cautiously to normotensive patients.
Patient Monitoring
Laboratory studies should include complete blood count (CBC); partial thromboplastin time; prothrombin time; fibrin degradation products; electrolytes; blood urea nitrogen (BUN); creatinine, glucose, calcium, and creatine kinase levels; liver function tests; arterial blood gases (ABGs); urinalysis; and ECG.
Monitor the cardiac rhythm continuously. If an infectious etiology is suspected, obtain appropriate cultures. If a central nervous system (CNS) etiology is considered likely, CT imaging followed by spinal fluid examination is appropriate.
Treat rhabdomyolysis or urine output of <30 mL/hr with adequate volume replacement, mannitol (12.5÷25 g IV), and bicarbonate (44÷100 mEq/L in 0.45% normal saline) to promote osmotic diuresis and urine alkalinization. Despite these measures, renal failure may still complicate 5% of cases of classic heat stroke and 25% of cases of exertional heat stroke.
Hypoxemia and acute respiratory distress syndrome (ARDS) may occur. Treat as described in Chapter 8, Critical Care.
Treat seizures with diazepam and phenytoin.
Provide supportive care for hepatic injury, congestive heart failure (CHF), and coagulopathy.
Cold-Induced Illness
General Principles
Exposure to the cold may result in several different forms of injury.
Risk factors are accelerated heat loss, which is promoted by exposure to high wind or by immersion.
Extended cold exposure may result from alcohol or drug abuse, injury or immobilization, and mental impairment.
Chilblains are among the mildest form of cold injury and result from exposure of bare skin to a cold, windy environment (33°÷60°F).
The ears, fingers, and tip of the nose typically are injured, with itchy, painful erythema on rewarming.
Treatment involves rapid rewarming (see Frostnip), moisturizing lotions, and analgesics and instruct the patient to avoid re-exposure.
Immersion injury (trench foot)
Immersion injury is caused by prolonged immersion (longer than 10÷12 hours) at a temperature <50°F.
Treat by rewarming followed by dry dressings. Treat secondary infections with antibiotics.
Frostnip is the mildest form of frostbite.
It occurs most frequently on the distal extremities, the nose, or the ear.
It is marked by tissue blanching and decreased sensitivity.
Rapid rewarming, in a water bath at 104°÷108°F (40°÷42°C), is the treatment of choice for all forms of frostbite. The water temperature should never be hotter than 112°F.
Superficial frostbite
Superficial frostbite involves the skin and subcutaneous tissues.
Areas with first-degree involvement are white, waxy, and anesthetic; have poor capillary refill; and are painful on thawing. Second-degree involvement is manifested by clear or milky bullae.
The treatment of choice is rapid rewarming. Immerse the affected body part for 15÷30 minutes; hexachlorophene or povidone-iodine can be added to the water bath. Narcotic analgesics may be necessary for rewarming pain. No deep injury ensues, and healing occurs in 3÷4 weeks.
Deep frostbite
General Principles
Deep frostbite involves death of skin, subcutaneous tissue, and muscle (third degree) or deep tendons and bones (fourth degree).
The tissue appears frozen and hard.
On rewarming, there is no capillary filling.
Hemorrhagic blisters form, followed by eschars. Healing is very slow, and demarcation of tissue with autoamputation may occur.
Diabetes mellitus, peripheral vascular disease, an outdoor lifestyle, and high altitude are additional risk factors. More than 90% of deep frostbite occurs at temperatures <6.7°C (44°F) with exposures longer than 7÷10 hours.
The treatment is rapid rewarming as described above. Rewarming should not be started until there is no chance of refreezing.
Administer analgesics (IV opioids) as needed.
Admit the patient to a surgical service.
Elevate the affected extremity, prevent weight bearing, separate the affected digits with cotton wool, prevent tissue maceration by using a blanket cradle, and prohibit smoking.
Update tetanus immunization.
Intra-arterial vasodilators, heparin, dextran, prostaglandin inhibitors, thrombolytics, and sympathectomy are not routinely justified.
Use antibiotics only for documented infection.
Amputation is undertaken only after full demarcation has occurred.
General Principles
Hypothermia is defined as a core temperature of <35°C (95°F).
Classification of severity by temperature is not universal. One scheme defines hypothermia as mild at 34°÷35°C, moderate at 30°÷34°C, and severe at <30°C.
The most common cause of hypothermia in the United States is cold exposure due to alcohol intoxication.
Another common cause is cold water immersion.
Differential Diagnosis
Cerebrovascular accident
Drug overdose
Diabetic ketoacidosis
Adrenal insufficiency
Monitor core temperature.
A standard oral thermometer registers only to a lower limit of 35°C. Monitor the patient continuously with a rectal probe with a full range of 20°÷40°C.
Equal efficacy of ear thermistor monitoring has not been demonstrated.
Clinical Presentation
Presentation varies with the temperature of the patient at presentation. All organ systems can be involved.
CNS effects
At temperatures below 32°C, mental processes are slowed and the affect is flattened.
At <32.2°C (90°F), the ability to shiver is lost, and deep tendon reflexes are diminished.
At 28°C, coma often supervenes.
Below 18°C, the electroencephalogram (EEG) is flat. On rewarming from severe hypothermia, central pontine myelinolysis may develop.
Cardiovascular effects
After an initial increased release of catecholamines, there is a decrease in cardiac output and heart rate with relatively preserved mean arterial pressure. ECG changes, manifest initially as sinus bradycardia with T-wave inversion and QT-interval prolongation, may progress to atrial fibrillation at temperatures of <32°C.
Osborne waves (J-point elevation) may be visible, particularly in leads II and V6.
An increased susceptibility to ventricular arrhythmias occurs at temperatures below 32°C.
At temperatures of <30°C, the susceptibility to ventricular fibrillation is increased significantly, and unnecessary manipulation or jostling of the patient should be avoided.
A decrease in mean arterial pressure may also occur, and, at temperatures of <28°C, progressive bradycardia supervenes.
Respiratory effects
After an initial increase in minute ventilation, respiratory rate and tidal volume decrease progressively with decreasing temperature.
ABGs measured with the machine set at 37°C should serve as the basis for therapy without correction of pH and carbon dioxide tension (PCO2).12,13
Renal manifestations
Cold-induced diuresis and tubular concentrating defects may be seen.
Laboratory Studies
Basic laboratory studies should include CBC; coagulation studies; liver function tests; BUN; electrolytes; creatinine, glucose, creatine kinase, calcium, magnesium, and amylase levels; urinalysis; ABGs; and ECG.
Obtain toxicology screen if mental status alteration is more profound than expected for temperature decrease.
Serum potassium often is increased.
Elevated serum amylase may reflect underlying pancreatitis.
Hyperglycemia may be noted but should not be treated, as rebound hypoglycemia may occur with rewarming.
DIC may also occur.
Obtain chest, abdominal, and cervical spine radiographs to evaluate all patients with a history of trauma or immersion injury.
Administer supplemental oxygen.
Give thiamine to most patients with cold exposure, as exposure due to alcohol intoxication is common.
Administration of antibiotics is a controversial issue; many authorities recommend antibiotic administration for 72 hours, pending cultures. In general, those patients with hypothermia due to exposure and alcohol intoxication are less likely to have a serious underlying infection than are those who are elderly or who have an underlying medical illness.
Special Therapy
Rewarming. The patient should be rewarmed with the goal of increasing the temperature by 0.5°÷2.0°C/hr, although the rate of rewarming has not been shown to be related to outcome.
Passive external rewarming
This method depends on the patient's ability to shiver.
It is effective only at core temperatures of 32°C or higher.
Remove wet clothing, cover patient with blankets in a warm environment, and monitor.
Active external rewarming
Application of heating blankets (40°÷45°C) or warm bath immersion. This type of therapy has been feared to cause paradoxical core acidosis, hyperkalemia, and decreased core temperature, as cold stagnant blood returns to the central vasculature,14 although Danish naval research supports arm and leg rewarming as effective and safe.15
Pending further investigation, active rewarming is best reserved for young, previously healthy patients with acute hypothermia and minimal pathophysiologic derangement.
Active core rewarming is preferred for treatment of severe hypothermia, although few data are available on outcomes.16
Heated oxygen is the initial therapy of choice for the patient whose cardiovascular status is stable. This therapeutic maneuver can be expected to raise core temperatures by 0.5°÷1.2°C/hr.17 Administration through an endotracheal tube results in more rapid rewarming than delivery via face mask. Administer heated oxygen through a cascade humidifier at a temperature of 45°C or lower.
IV fluids can be heated in a microwave oven or delivered through a blood warmer; give fluids only through peripheral IV lines.
Heated nasogastric or bladder lavage is of limited efficacy because of low exposed surface area and is reserved for the patient with cardiovascular instability.
Heated peritoneal lavage with fluid warmed to 40°÷45°C is more effective than is heated aerosol inhalation, but it should be reserved for patients with cardiovascular
instability. Only those who are experienced in its use should perform heated peritoneal lavage, in combination with other modes of rewarming.
Closed thoracic lavage with heated fluid by thoracostomy tube has been recommended but is unproved.18
Hemodialysis can be used for the severely hypothermic, particularly when due to an overdose that is amenable to treatment in this way.
Extracorporeal circulation (cardiac bypass) is used only in hypothermic individuals who are in cardiac arrest; in these cases, it may be dramatically effective.19 Extracorporeal circulation may raise the temperature as rapidly as 10°÷12°C/hr but must be performed in an intensive care unit (ICU) or operating room.
Maintain airway and administer oxygen.
If intubation is required, the most experienced operator should perform it (see Airway Management and Tracheal Intubation in Chapter 8, Critical Care).
Conduct cardiopulmonary resuscitation (CPR) in standard fashion. Perform simultaneous vigorous core rewarming; as long as the core temperature is severely decreased, it should not be assumed that the patient cannot be resuscitated. Reliable defibrillation requires a core temperature of 32°C or higher; prolonged efforts (to a core temperature of 35°C) may be justified because of the neuroprotective effects of hypothermia. Do not begin CPR if an organized ECG rhythm is present, as inability to detect peripheral pulses may be due to vasoconstriction, and CPR may precipitate ventricular fibrillation.
Do not perform Swan-Ganz catheterization, as it may precipitate ventricular fibrillation.
If ventricular fibrillation occurs, begin CPR as per the advanced cardiac life support (ACLS) protocol. Amiodarone may be administered as per the protocol, although there is no evidence to support its use or guide dosage; some experts suggest reducing the maximum cumulative dose by half. Avoid procainamide because it may precipitate ventricular fibrillation and increase the temperature that is necessary to defibrillate the patient. Rewarming is key.
Monitor ECG rhythm, urine output, and, possibly, central venous pressure in all patients with an intact circulation.
Admit patients with an underlying disease, physiologic derangement, or core temperature <32°C, preferably to an ICU.
Discharge individuals with mild hypothermia (32°÷35°C) and no predisposing medical conditions or complications when they are normothermic and an adequate home environment can be ensured.
General Principles
Near-drowning is defined as survival for at least 24 hours after submersion in a liquid medium.
Risk factors include youth, inability to swim, alcohol and drug use, barotrauma (in scuba diving), head and neck trauma, and loss of consciousness associated with epilepsy, diabetes, syncope, or dysrhythmias.
Much has been made of the differences in pathophysiology between fresh- and salt-water drownings. However, the major insults [i.e., hypoxemia and tissue hypoxia related to ventilation-perfusion (V/Q) mismatch, acidosis, and hypoxic brain injury with cerebral edema] are common to both.
Hypothermia, pneumonia, and, rarely, DIC, acute renal failure, and hemolysis also may occur.
Laboratory Studies
Obtain serum electrolytes, CBC, and ABGs. Monitor the cardiac rhythm continuously. Obtain blood alcohol level and drug screen if the mental status is not normal.
Obtain chest radiograph.
Obtain ECG.
Begin with resuscitation, focusing on airway management and ventilation with 100% oxygen.
Establish an IV line with 0.9% saline or lactated Ringer solution.
The Heimlich maneuver is not indicated unless upper airway obstruction is present.21
Immobilize the cervical spine, as trauma may be present.
Treat hypothermia vigorously (see Cold-Induced Illness).
Reserve antibiotics for documented infection. Pneumonia may be due to water-borne organisms such as Pseudomonas, Aeromonas, and Proteus.
Prophylactic glucocorticoids have no role.21
Cerebral edema
Cerebral edema may occur suddenly within the first 24 hours and is a major cause of death. Treatment of cerebral edema does not appear to increase survival,22 and intracranial pressure monitoring does not appear to be effective. Nevertheless, if cerebral edema occurs, hyperventilate the patient to a PCO2 not lower than 25 mm Hg (to avoid excessive vasoconstriction), and administer mannitol (1÷2 g/kg q3÷4h) or furosemide (1 mg/kg IV q4÷6h).
Treat seizures aggressively with phenytoin.
The routine administration of glucocorticoids is not recommended.
Hypothermia or barbiturate “coma” is not indicated.23
It may be necessary to sedate and paralyze the patient to reduce oxygen consumption and facilitate intracranial pressure management.
Pulmonary complications
Administer 100% oxygen initially, titrating thereafter by ABGs.
Intubate the patient endotracheally and begin mechanical ventilation with positive end-expiratory pressure (PEEP) if the patient is apneic, is in severe respiratory distress, or has oxygen-resistant hypoxemia.
Administer bronchodilators if bronchospasm is present.
Artificial surfactant has not been shown to be useful.24,25
Metabolic complications
Manage metabolic acidosis with mechanical ventilation, sodium bicarbonate (if the pH is persistently <7.2), and BP support.
Admit patients who have survived severe episodes of near-drowning to an ICU. Noncardiogenic pulmonary edema may still develop in those individuals with less severe immersions.
Admit any patient with pulmonary signs or symptoms, including cough, bronchospasm, abnormal ABGs or oxygen saturation as measured by pulse oximetry (SpO2), or abnormal chest radiograph.
Observe the asymptomatic patient with a questionable or brief water immersion for 4÷6 hours and discharge the patient if the chest radiograph and ABGs are normal.26 However, if a documented long submersion, unconsciousness, initial cyanosis or apnea, or even a brief requirement for resuscitation has occurred, the patient must be admitted for at least 24 hours.
General Principles
Recognition of poisoning and medication overdose requires a high index of suspicion and careful clinical evaluation. In the most recent year for which information is available, more than 2.4 million toxic exposures occurred in the United States, resulting in 1,183 deaths.27 Of these exposures, nearly 200,000 were suicidal (accounting for over half the deaths), about 46,000 due to drug abuse, and over 9,000 malicious (e.g., date-rape drugs).
Up to 50% of all initial poisoning histories may be incorrect. The ingestion of multiple drugs is common.
Seek identification of the drug or drugs ingested and their dosages from the patient's family or friends, private physician, pharmacist, and paramedical personnel. Obtain supporting materials (e.g., pill bottles) and clues regarding the timing of ingestion.
Recognition of specific toxic syndromes is often helpful in directing initial management (Table 25-1).
Clinical Presentation
Pay particular attention to vital signs, neurologic status, pupillary reactions, cardiovascular response, abdominal findings, and unusual odors and excreta.
Laboratory Studies
ABGs, serum electrolytes, and acid-base abnormalities may suggest a particular toxin.
Order baseline screening of liver and kidney function.
Screening of blood, urine, and gastric aspirate for specific toxic agents is important, but, in most cases, therapy must proceed before such results are available.
Perform a pregnancy test in women of child-bearing years
Abdominal radiography may be useful in detecting retained pills (such as iron).
Obtain an ECG and monitor the cardiac rhythm continuously until the ingested agent is identified and thereafter as appropriate.
Although the computerized Poisindex (2006; Micromedex, Greenwood Village, CO) system is helpful, seek additional specific advice from the regional poison control center.
Supportive care is crucial. Maintain a patent airway and adequate ventilation. Intubate the trachea if airway protection is required.
Hypotension usually responds to IV fluids, although vasopressors may be required in refractory cases or in the presence of pulmonary edema. Use dopamine in most situations; choose norepinephrine for overdoses with α antagonists (phenothiazines) and tricyclic antidepressants (due to the proarrhythmic effect of dopamine).
Arrhythmias may be related to cardiac or autonomic effects; treatment depends on the toxin.
CNS depression or coma occurs frequently.
When present, administer naloxone (2 mg IV) for possible narcotic overdose, give 50% dextrose in water (50 mL IV) or determine finger-stick glucose immediately, administer thiamine (100 mg IV push) for possible Wernicke-Korsakoff's syndrome, and give oxygen for possible carbon monoxide intoxication.
Give flumazenil for known or suspected benzodiazepine overdose. However, do not give it for unknown overdoses, as this agent may precipitate seizures in cyclic antidepressant overdose. Also, avoid flumazenil administration in patients who have ingested drugs that are known to cause seizures (cocaine, lithium, theophylline, isoniazid, cyclosporine) or who are known to have a pre-existing seizure disorder.28
Prevention of Further Drug Absorption
Prevention of further drug absorption has traditionally been thought to be facilitated by gastric emptying (gastric lavage, induced emesis), followed by administration of activated charcoal.
Gastric emptying procedures, if used, should be initiated within 1 hour of the ingestion.
Because most adult overdose patients present several hours after toxic ingestion and because the use of syrup of ipecac may delay subsequent therapy, administration of activated charcoal alone is recommended as the primary gastrointestinal (GI) decontamination procedure for most patients.29
No difference in outcome appears to occur whether gastric emptying plus charcoal or charcoal administration alone is used.30,31 Theoretic exceptions may include phenothiazine overdose (delayed gastric emptying) and drugs that form gastric concretions.
TABLE 25-1 Toxic Syndromes and Possible Causes
Possible causes
Acquired hemoglobinopathies
Dyspnea, cyanosis, confusion or lethargy, headache
Carbon monoxide
Methemoglobinemia (nitrites, phenazopyridine)
Anion-gap metabolic acidosis
Ethylene glycol
Dry mouth and skin, blurred vision, mydriasis, tachycardia, generalized sunburnlike rash or flushing of skin, hyperthermia, abdominal distention, urinary urgency or retention, confusion, hallucinations, delusions, excitation, or coma
Atropine and other belladonna alkaloids
Jimson seeds
Hypersalivation, bronchorrhea, bronchospasm, urination or defecation, neuromuscular failure, lacrimation
Organophosphate insecticides
Wild mushrooms
Nausea, vomiting, collapse, coma, bradycardia, no cyanosis, decreased arteriovenous O2 difference with severe metabolic acidosis
Dysphoria and dysphagia, trismus, oculogyric crisis, rigidity, torticollis, laryngospasm
Chlorpromazine and other antipsychotics
Other phenothiazines
Central nervous system depression, respiratory depression, miosis, hypotension
Morphine and heroin
Other synthetic and semisynthetic opiates
Fever, hyperpnea, respiratory alkalosis or mixed acid-base disturbance, hypokalemia, tinnitus
Other salicylate products
Excitation, hypertension, cardiac arrhythmias, seizures
β Agonists, inhaled or injected
Source: Modified from Quick G, Crocker PJ. Toxic emergency: agent unknown. Emerg Decisions 1986;7:44. Reprinted with permission from Physicians World/Thomson Healthcare, Secaucus, NJ.
 Activated charcoal
Treatment adsorbs most drugs, preventing further absorption from the GI tract. Exceptions include alkalis, arsenic and other heavy metals, hydrocarbons, cyanide, ethanol (EtOH) and other alcohols, lithium, ferrous sulfate, carbamate, and mineral acids. It is not indicated for these ingestions.
Activated charcoal also promotes efflux of selected drugs (theophylline, phenobarbital, and carbamazepine) from the blood into the bowel lumen.
Do not use activated charcoal when bowel obstruction or perforation is present or when endoscopy is contemplated.
When repeated dosing is used, no more than a single dose of sorbitol or other cathartic should be given. Although multidose charcoal has been shown to increase selected drug elimination significantly, it has not yet been demonstrated in a controlled study to reduce mortality in poisoned patients.
It is indicated in ingestions of life-threatening amounts of carbamazepine, phenobar- bital, theophylline, quinine, dapsone, paraquat, and Amanita phalloides.33,34 It may be of use in overdoses of amitriptyline, cyclosporine, dextropropoxyphene, diazepam, digitoxin, digoxin, disopyramide, methotrexate, nadolol, phencyclidine, phenylbutazone, phenytoin, piroxicam, sotalol, and valproate. Its use in salicylate overdose is controversial.
Give an initial dose of 50÷100 g and repeat that dose every 4 hours until the patient's condition and laboratory parameters improve. Prehospital administration further enhances recovery. Evidence to support its use more than 1 hour after toxic ingestion is unavailable, and many experts do not recommend its administration after that interval.32 If the patient is obtunded or has an absent gag reflex, the airway must be protected; endotracheal intubation may be necessary.
Because there is no evidence to show that administration of ipecac improves outcome and there is some evidence to suggest an increase in complications,35 and because of its many contraindications, routine use in the emergency center has largely been abandoned.36
Contraindications to ipecac use include decreased level of consciousness, absent gag reflex, caustic ingestion, convulsions or exposure to a substance that is likely to cause convulsions, and medical conditions that make emesis unsafe. Do not give ipecac for ingestion of unknown toxins, as aspiration may occur if coma or seizures develop.
Gastric lavage
Gastric lavage should not be used routinely in the management of the poisoned patient. Exceptions include ingestions of a life-threatening amount of toxin when the patient presents within 60 minutes37 or when concretions are believed to be present. Use a large orogastric tube (No. 28÷36 Fr.) for these patients.
Contraindications include corrosive ingestion. Lavage should not be performed with an unprotected airway if the patient has lost airway protective reflexes or has ingested hydrocarbons with a high aspiration potential. In these cases, lavage should be performed only after endotracheal intubation. Lavage with 200-mL boluses of warm saline, repeated until the effluent is clear, and follow this by instillation of activated charcoal.
The use of a cathartic is not supported by clinical evidence and is therefore not routinely recommended.38 If used, give no more than a single dose.
Acceptable forms:
Magnesium citrate, 4 mL/kg (300 mL maximum)
Sorbitol, 1÷2 g/kg (150 g maximum)
Magnesium or sodium sulfate, 25÷30 g
Do not give magnesium salts to patients with renal failure.
Whole-bowel irrigation
Commercially available polyethylene glycol bowel preparation solution should not be used routinely in the management of the poisoned patient,39 as there is no conclusive evidence that it improves outcomes.
Exceptions can be considered for toxic ingestions of sustained-release drugs such as β-adrenergic antagonists, calcium channel antagonists, lithium, and theophylline.
Evidence is insufficient either to support or exclude its use for iron ingestion with radiographically persistent tablets in the GI tract or body packing with heroin or cocaine.
It is contraindicated in the presence of bowel obstruction, ileus, intestinal perforation, and hemodynamic instability and should not be administered to a patient with a compromised unprotected airway.
Administer 1÷2 L/hr to a total of 10 L; it can be discontinued earlier if the rectal effluent is clear. Obtain an abdominal radiograph to document clearance of iron or drug-containing packets.
Endoscopic or surgical removal, or both
These should be considered only for ingestion of life-threatening agents that have not been or cannot be effectively removed by the above measures, such as button batteries lodged in the esophagus and pharmacobezoars of highly toxic materials and for cocaine body packers with severe toxicity due to rupture of a packet.
Endoscopy should not be performed to remove unruptured drug packets, as this intervention may result in rupture and greater toxicity.
Removal of Absorbed Drugs
Removal can be achieved by enhancement of renal excretion and extracorporeal methods.
Use forced diuresis only when specifically indicated because of the risk of causing acid-base disturbances, electrolyte abnormalities, and cerebral or pulmonary edema. Do not attempt forced diuresis in patients with renal insufficiency, cardiac disease, or existing electrolyte abnormalities. Few data support the efficacy of this procedure in improving survival.
Forced alkaline diuresis, achieving a urinary pH of 7.5÷9.0, promotes excretion of drugs that are weak acids, such as salicylates, barbital, and phenobarbital. Administer a solution of sodium bicarbonate, 44÷100 mEq, added to 1 L 0.45% saline, at 250÷500 mL/hr for the first 1÷2 hours. Concomitant administration of potassium chloride may be necessary to treat diuresis-induced hypokalemia and to achieve urinary alkalinization. Exercise great care to avoid excessive volume expansion, especially in the elderly. Administer maintenance alkaline solution and diuretics to maintain a urinary output of 2÷3 mL/kg/hr.
Forced acid diuresis is not recommended for any agent.
Extracorporeal Removal of Specific Toxins by Hemodialysis or Hemoperfusion
Hemodialysis or hemoperfusion may be used when:
Clinical deterioration persists despite intensive supportive therapy
Blood levels reach potentially lethal concentrations
A risk of lethal delayed effects exists
Renal or hepatic failure impairs clearance of toxin. Common toxins that can be removed by hemodialysis include toxic alcohols, salicylates, theophylline, and lithium. Generally, compounds with low molecular weight, small volume of distribution, and low degree of protein binding of drug are amenable to removal by hemodialysis.
Specific antidotes are available that neutralize or prevent the toxic effect of certain drugs (Table 25-2). For information on the pharmacokinetics of the offending agent and specific treatment guidelines, contact the regional poison control center immediately if the drug that was ingested is known.
Observe even those patients with apparently trivial overdoses of potentially toxic agents for at least 4 hours before contemplating their discharge. Do not discharge any patient
who has taken an intentional overdose without formal psychiatric consultation and assessment of disposition.
Refer individuals who experience inadvertent recreational drug overdose for counseling and, possibly, detoxification.
Patients who are considered potentially suicidal require constant one-on-one supervision while on the medical service.
General Principles
Acetaminophen is a common ingredient in many analgesic and antipyretic preparations. Because of this, ingredients of over-the-counter medications taken in overdose should be examined carefully.
Hepatic toxicity is due to depletion of hepatic glutathione and subsequent accumulation of a toxic intermediate metabolite, N-acetyl-p-benzoquinoneimine. Toxicity usually occurs after acute ingestion of more than 140 mg/kg, or at least 7.5 g. Precise determination of probable toxicity can be obtained by plotting a plasma acetaminophen level (drawn at least 4 hours after ingestion) on a nomogram in relation to the time since ingestion (Fig. 25-1). However, nearly half of hospitalizations for acetaminophen toxicity are due to toxicity from chronic ingestion, which is increased in those with excess alcohol intake.40
The nomogram does not provide useful information regarding toxicity of chronic ingestion, however. In this instance, treatment is recommended if there is evidence of liver toxicity and the acetaminophen level is >10 mcg/mL. If in doubt, consult with an expert in clinical toxicology or hepatology, or both.
The nomogram is also of uncertain usefulness in acute overdose of sustained-release products. In this latter situation, the Rocky Mountain Poison Center recommends that a second drug level be obtained 4÷6 hours after the first; if either level falls in the possibly toxic range, antidotal therapy is advised.41
Symptoms during the first 24 hours include anorexia, vomiting, and diaphoresis.
Hepatic enzymes begin to rise 24÷36 hours after ingestion and peak (aspartate aminotransferase earliest) 72÷96 hours after ingestion. Recovery starts after approximately 4 days unless hepatic failure develops.
Treatment includes supportive measures and GI decontamination.
Gastric lavage is not indicated.
Do not administer ipecac, as its use delays administration of the specific antidote.
Administer activated charcoal as soon as possible after the ingestion. Charcoal appears to provide an additional hepatoprotective effect.42
When the history suggests that a toxic dose has been ingested, do not wait for return of the blood acetaminophen level to administer the first dose of acetylcysteine (Mucomyst), a specific antidote that acts as a glutathione substrate. This antidote is most effective in preventing hepatotoxicity if given within 8 hours of ingestion and is recommended up to 24 hours; it may be helpful when administered up to 36 hours after the event if hepatotoxicity is evident.43
The initial dose is 140 mg/kg diluted to a 5% solution in a soft drink, juice, or water, given PO or by gastric tube; it can be given simultaneously with charcoal without impairment of its efficacy.
Subsequent administration (70 mg/kg q4h for a total of 17 doses) is directed by the initial plasma acetaminophen level. If a toxic level is detected, give the full 17 doses; if not, no further antidote is indicated. If vomiting occurs <1 hour after administration of the antidote, repeat the dose.
If vomiting is repetitive and interferes with acetylcysteine administration, use metoclopramide or droperidol, or administer acetylcysteine via a fluoroscopically placed nasoduodenal tube over a period of 30÷60 minutes.
IV acetylcysteine is now U.S. Food and Drug Administration (FDA) approved and available commercially as Acetadote®. It should be considered for those who cannot or will not take oral acetylcysteine or who have bowel obstruction, GI bleeding, or fulminant hepatic failure.
It should be considered for use in the pregnant patient. The initial dosage is 150 mg/kg IV over 1 hour in 200 mL 5% dextrose in water (D5W), followed by 50 mg/kg in 500 mL over 4 hours, followed by 100 mg/kg in 500 mL over 16 hours.
Side effects include bronchospasm, rash, flushing, and anaphylactoid reaction and are generally dose related. Flushing requires no treatment; treat urticaria with diphenhydramine. Give albuterol and corticosteroids for bronchospasm. Treat angioedema with diphenhydramine, epinephrine, and corticosteroids. Consider administration of IV cimetidine. Administration of acetylcysteine can be safely resumed 1 hour after successful treatment.44
Obtain baseline aspartate transaminase (AST), alanine transaminase (ALT), bilirubin level, BUN, and prothrombin time or international normalized ratio (INR) and repeat these readings at least daily for 3 days. Obtain hepatology consultation for consideration of orthotopic liver transplantation if there is biochemical evidence of hepatic failure. Transplantation is considered if the pH is <7.3 after 24 hours or the prothrombin time is >100 seconds (international normalized ratio >6.5) and grade 3÷4 coma is present and the creatinine is >3.4 mg/dL.
Cyclic Antidepressants
General Principles
Traditional tricyclic antidepressants include amitriptyline, imipramine, desipramine, nortriptyline, doxepin, and protriptyline.
Pharmacologic actions include central and peripheral anticholinergic activity, depression of myocardial contractility, slowing of intraventricular and atrioventricular conduction, and CNS effects that are similar to those of phenothiazines. Despite the widespread use of the much safer selective serotonin reuptake inhibitor antidepressants, overdose with cyclic antidepressants is still the third-leading cause of drug overdose÷related death in the United States.27
Overdoses of <20 mg/kg cause few fatalities; 35 mg/kg is the approximate median lethal dose, and overdoses in excess of 50 mg/kg are likely to result in death.
Next-generation cyclic antidepressants include amoxapine and loxapine (tricyclics with diminished cardiovascular toxicity but increased propensity to severe seizures), maprotiline (a tetracyclic with greater seizure proclivity and cardiovascular toxicity similar to that of older tricyclics), mianserin (a tetracyclic with low propensity for cardiovascular or neurologic toxicity), and trazodone (a noncyclic with minimal cardiovascular and CNS toxicity).
Still newer antidepressants include mirtazapine, venlafaxine, bupropion, and nefazodone. Limited data suggest that mirtazapine is relatively nontoxic in overdose.45 Venlafaxine is also relatively nontoxic in overdose.
Clinical Presentation
Clinical manifestations include evidence of cholinergic blockade (mydriasis, ileus, urinary retention, and hyperpyrexia).
Cardiovascular toxicity occurs as a result of anticholinergic, catecholamine-related, quinidinelike, and α-antagonist effects; these effects result in supraventricular and ventricular arrhythmias, including torsades de pointes, conduction blocks, hypotension, hypoperfusion, and pulmonary edema.
CNS manifestations range from initial agitation to confusion, stupor, and coma. Seizures may occur, and the resultant metabolic acidosis may worsen cardiac toxicity.
Symptoms of bupropion overdose include labored breathing, salivation, arched back, ataxia, and convulsions. Symptoms of nefazadone overdose include drowsiness, vomiting, hypotension, tachycardia, incontinence, and coma.
Laboratory Studies
Laboratory studies aid in assessing the severity of the condition and in monitoring progress. Plasma levels correlate poorly with severity of symptoms, although blood levels >1,000 ng/mL have a higher risk of cardiac toxicity. ABGs are useful for ensuring adequate gas exchange and for monitoring alkalinization. ECGs showing limb-lead QRS duration of >100 ms are predictive of seizures; duration >160 ms predicts ventricular dysrhythmias; a terminal 40-ms QRS axis that is more rightward than 120 degrees is even more sensitive.46,47
The course of therapy includes supportive measures and GI decontamination.
Do not administer ipecac syrup, as obtundation may occur rapidly and promote aspiration.
Gastric lavage theoretically may be performed regardless of the time of presentation, as cyclic antidepressants delay gastric emptying; however, clinical studies do not show a difference in patients treated in this way versus those given activated charcoal only.48
Repetitive administration of activated charcoal, 50 g PO or per tube q2÷4h, is not routinely recommended.
Forced diuresis and hemodialysis are not indicated. Resin or charcoal hemoperfusion removes <1%÷3% of body burden, but this reduction may be associated with improvement of life-threatening cardiac or CNS complications.
Continuous cardiac monitoring is mandatory. Cyclic antidepressants are protein bound in an alkaline environment and are toxic in an acid environment. Cardiac (and CNS) toxicity therefore is enhanced by metabolic or respiratory acidosis. Initiate treatment prophylactically, as toxic complications often are refractory to therapy once they have developed.
Induce alkalinization with IV sodium bicarbonate, 1÷2 mEq/kg, to maintain an arterial pH of 7.45÷7.55. Such an alkaline pH is effective in preventing and treating hypotension, arrhythmias (ventricular and supraventricular), and conduction disturbances. If the patient is intubated, hyperventilate to a PCO2 of no lower than 25 mm Hg and an arterial pH of 7.45÷7.55, as this is an effective means of alkalinization and avoids the administration of large amounts of sodium.
Manage ventricular arrhythmias refractory to alkalinization with lidocaine or phenytoin (see Chapter 7, Cardiac Arrhythmias). TypeIa antiarrhythmics (procainamide, quinidine, or disopyramide) are contraindicated because of additive toxicity. Treat torsades de pointes with magnesium, isoproterenol, and atrial overdrive pacing (see Chapter 7, Cardiac Arrhythmias). Do not use physostigmine unless all other measures for life-threatening arrhythmias have failed. Use temporary ventricular pacing for complete heart block. Treat hypotension that is unresponsive to alkalinization with norepinephrine and fluid administration.
CNS complications. Alkalinization does not reverse CNS complications. Physostigmine (2 mg IV over 1 minute) reverses CNS depression rapidly in patients with pure cyclic antidepressant overdose. However, because repeated doses are necessary and physostigmine may cause dysrhythmias and seizures, its use is not recommended for coma. Supportive care of coma usually is adequate. Treat seizures with diazepam and phenytoin (see Chapter 24, Neurologic Disorders). Barbiturates are preferred over phenytoin for drug-induced seizures by some but not all authorities. Status epilepticus should be treated aggressively, including the use of high-dose barbiturates, paralysis, and general anesthesia, to prevent permanent neurologic damage. Treat hyperthermia by cooling.
Respiratory depression. Treat this commonly occurring complication with endotracheal intubation and mechanical ventilation. Pulmonary edema and aspiration also are common.
Disposition. Patients should be admitted to an ICU if they have a depressed level of consciousness, respiratory depression, hypotension, arrhythmia, conduction blocks (including QRS >100 ms), or seizures. Observe any asymptomatic individual with a normal ECG in the emergency department and perform cardiac monitoring of such a patient for 6 hours. If the patient remains asymptomatic, the ECG remains normal, and bowel sounds are normal, the patient may safely undergo assessment for psychiatric disposition. If any signs or symptoms are present, the patient must be admitted. Caution is imperative: 25% of fatalities occur in patients who are awake and alert at the time of presentation, and three-fourths of these patients are in normal sinus rhythm. After a patient's admission, criteria for discharge from an ICU include normal mental status, absence of all cyclic antidepressant symptoms, and no ECG abnormalities (including sinus tachycardia) for 24 hours. Significant arrhythmias rarely develop in a patient who meets all these criteria.
Selective Serotonin Reuptake Inhibitors
Commonly available selective serotonin reuptake inhibitors (SSRIs) include fluoxetine, sertraline, paroxetine, fluvoxamine, and citalopram.
Symptoms are usually minimal.
Patients may become agitated or drowsy or, occasionally, confused.
Ataxia, vertigo, tremor, delusions, or hallucinations may occur, as may nausea and emesis.
Seizures are rare, occurring most often after fluoxetine or citalopram overdose.49,50
Tachycardia is noted frequently; however, ECG changes and significant cardiovascular toxicity are uncommon, although severe citalopram overdose may have QT prolongation. Fatalities are rare.51
Simultaneous ingestion of these drugs with tricyclic antidepressants may raise plasma levels of the tricyclic. If they are ingested with other drugs that cause serotonin release, such as clomipramine, monoamine oxidase inhibitors, and l-tryptophan, the serotonin syndrome may result.
Avoid emesis. GI lavage may be considered if the patient presents <1 hour after ingestion. Administer activated charcoal. Although cardiovascular and CNS toxicity rarely occur, obtain an ECG as a baseline.
Admit patients who have taken large overdoses to a medical floor, particularly if they are symptomatic or if there is coingestion. Treat seizures with diazepam and phenytoin.
If the patient is asymptomatic and medically stable after 6 hours of observation, psychiatric evaluation and disposition assessment can be made safely.
Serotonin Syndrome
Serotonin syndrome occurs most frequently after ingestion of two or more drugs that increase serotonin levels by different mechanisms.
Examples include monoamine oxidase inhibitors, l-tryptophan, amphetamines, cocaine, 3,4-methylenedioxymethamphetamine (MDMA), fenfluramine, serotonin reuptake inhibitors, tricyclic antidepressants, sumatriptan, amantadine, levodopa, and bromocriptine.
Symptoms include agitation, confusion, hallucinations, myoclonus, diaphoresis, tremor, shivering, nystagmus, diarrhea, and fever. Drowsiness may progress to coma. Seizures may occur.
Autonomic effects include tachycardia, hypertension, tachypnea, mydriasis, flushing, salivation, abdominal pain, hyperreflexia, and diarrhea.
Hyperthermia is characteristic. Rigidity, trismus, and opisthotonus may be present.
Severe complications include DIC, rhabdomyolysis and renal failure, respiratory failure, and ARDS.
Treatment is supportive with the administration of activated charcoal.
Emesis should not be induced.
Consider benzodiazepines for agitation.
Treat hyperthermia with cooling.
Diazepam and phenytoin can be given for seizures.
Hypertension can be treated with sedation and, if necessary, nitroprusside. If IV saline is unsuccessful for hypotension, administer norepinephrine.
Protect the airway and provide ventilatory support for respiratory failure.
Consider the administration of cyproheptadine, 4÷8 mg q1÷4h, until improvement occurs or a total of 32 mg is given.
Cardiovascular Drugs
β-Adrenergic Antagonists
General Principles
Symptoms usually occur within 2 hours of ingestion.
Cardiovascular manifestations include bradycardia, atrioventricular block, hypotension, and depression of cardiac function, which results in CHF. Sotalol may cause QT prolongation and torsades de pointes. Bradycardia occurs early but does not predict more serious cardiac disturbances.
Although some β1-specific agents may have little respiratory effect at the standard dosage in patients with asthma or chronic obstructive pulmonary disease, severe bronchospasm may result from ingestion of any β-adrenergic antagonist, because β1 selectivity is lost at high doses.
CNS manifestations include drowsiness, coma, hypoventilation, and seizures (caused most frequently by propranolol).
Nausea and vomiting may occur, and mesenteric ischemia may be severe, particularly with propranolol ingestion, as a result of decreased cardiac output and unopposed α-agonist activity.
β-Adrenergic antagonist overdose may cause hypoglycemia by blockade of counterregulatory mechanisms and may also make the appreciation of hypoglycemic symptoms more difficult.
Renal failure may occur as a result of hypotension.
Laboratory Studies
Measurement of serum drug levels is not useful. Obtain serum glucose and electrolyte levels. Record a baseline ECG and monitor cardiac activity continuously.
Establish an IV line before any other therapy is undertaken.
Consider gastric lavage if the patient is seen within 1 hour of ingestion of a potentially life-threatening amount, and administer activated charcoal. A second dose of activated charcoal for sustained-release preparation overdose has been recommended by some because of the theoretical potential for drug desorption, but there is no clinical evidence to support this.
Do not give syrup of ipecac because of the rapidity with which cardiac compromise may occur. Moreover, the increase in vagal tone associated with emesis may promote cardiovascular collapse.
If the patient becomes bradycardic or has other manifestations of a vagal reaction, administer up to 2 mg atropine IV.
Consider multidose charcoal for sotalol ingestion.
Treat hypotension with IV saline; hemodynamic monitoring may be necessary to gauge optimal fluid resuscitation.
Glucagon (50÷150 mcg/kg IV over 1 minute, followed by 1÷5 mg/hr in 5% dextrose) increases cardiac contractility and heart rate and is the drug of first choice for β-adrenergic antagonist overdose.
Isoproterenol (2÷20 mcg/min) may be useful, but high doses (200 mcg/min) may be necessary.
If the BP does not improve or falls, add norepinephrine.
Use epinephrine with caution, particularly with propranolol overdoses, because of the propensity for hypertension and reflex bradycardia.
Calcium chloride 10%, 10 mL IV, may also be useful for refractory propranolol overdose.
Consider intra-aortic balloon pump for refractory hypotension.
For torsades de pointes associated with sotalol overdose, isoproterenol, magnesium, and overdrive pacing may be useful (see Chapter 7, Cardiac Arrhythmias). A pacemaker may be necessary for severe bradycardia or heart block that is unresponsive to medications.
Use β-adrenergic agonists and theophylline for bronchospasm.
Treat seizures with IV benzodiazepine followed by IV phenytoin.
Treat hypoglycemia with IV glucose and, if resistant, IV glucagon.
Severe respiratory depression may require mechanical ventilation.
Dialysis may be useful in removal of nadolol, sotalol, atenolol, and acebutolol but is ineffective for propranolol, metoprolol, and timolol.
Disposition. Obtain a baseline ECG and monitor the patient's rhythm for at least 6 hours, even in the absence of symptoms. If any cardiovascular, respiratory, or neurologic symptoms are present, admit the patient to an ICU for therapy and continuous monitoring. If, however, no toxic symptoms have occurred 6 hours after ingestion, disposition guided by psychiatric consultation can be made safely.
Calcium Channel Antagonists
General Principles
Manifestations of calcium channel antagonist overdose depend on the drug ingested. Hypotension is common, as are nausea and vomiting.
Severe bradycardia, atrioventricular block, and asystole are most common after verapamil and diltiazem overdose and less common with the dihydropyridines (e.g., nifedipine, nicardipine, amlodipine), which are more likely to cause reflex tachycardia.
Pulmonary edema is most likely to occur after verapamil overdose, as is hypocalcemia. Lethargy, confusion, and coma are common. Seizures are most often due to verapamil, less common with diltiazem, and rare with nifedipine. Hyperglycemia occurs frequently.
Cardiovascular manifestations usually are apparent within 1÷5 hours after ingestion and may persist for more than 24 hours.
Sustained-release preparations, particularly verapamil, may cause rhythm disturbances up to 7 days after ingestion.
Laboratory Studies
Obtain serum calcium, magnesium, electrolyte, and glucose levels.
Blood levels of the drugs are not generally available or useful.
Obtain an ECG and monitor the cardiac rhythm. Monitor oxygenation by pulse oximetry, and obtain a chest radiograph.
Gastric decontamination
Avoid inducing emesis because of the potential for rapid cardiovascular collapse and aspiration.
If the patient presents soon after ingestion, consider gastric lavage followed by administration of charcoal.
Consider gastroscopy or whole-bowel irrigation with polyethylene glycol solution for removal of retained sustained-release tablets.
A second dose of activated charcoal for sustained-release preparation overdose has been recommended by some because of the theoretical potential for drug desorption, but there is no clinical evidence to support this.
Treat hypotension with IV 0.9% saline; if resistant, give IV dopamine.
Administer 10% calcium chloride (10÷20 mL IV) for hypotension, bradycardia, or heart block. Repeat at 10-minute intervals three to four times as necessary.
Calcium gluconate (3 g) is preferred when the patient is severely acidotic. A calcium gluconate drip at up to 2 g/hr can be titrated to BP, with monitoring of ECG and serum calcium.
Glucagon (50÷150 mcg/kg IV over 1 minute followed by 1÷5 mg/hr) may also be useful for heart block and hypotension.
Insulin infusion, 0.1÷1.0 unit/kg/hr with sufficient dextrose to maintain a normal blood glucose, has also been reported to be successful.
If hypotension is resistant to the preceding measures, arrange for placement of an intra-aortic balloon pump.
Atropine (up to 2 mg IV) can also be given for bradycardia or atrioventricular block, although it rarely is successful.
Isoproterenol is a less desirable alternative.
Place a transvenous pacemaker for medication-resistant heart block.
Treat seizures with an IV benzodiazepine (diazepam or lorazepam; see Chapter 24, Neurologic Disorders) and phenytoin.
Hemodialysis and hemoperfusion are not useful to accelerate drug removal.
Disposition. Admit all patients who have cardiovascular symptoms or seizures or who have ingested a sustained-release preparation to an ICU for continuous cardiovascular monitoring. If the patient has taken a non÷sustained-release preparation and is asymptomatic, obtain a baseline ECG and monitor ECG rhythm for at least 8 hours. If, at that point, the patient is completely asymptomatic and has a normal ECG, consider discharge after psychiatric consultation.
See Chapter 7, Cardiac Arrhythmias, for details; for doses of Fab' fragments, see Table 25-2.
Caustic ingestions
Alkaline Ingestions
Substances include liquid and crystalline lye, automatic dishwasher detergents, oven cleaners, hair relaxers, and some toilet bowl cleaners.
Strong alkali solutions, such as liquid drain cleaner, are the agents most commonly associated with injury.
Symptoms and Signs
Deep tissue injury in the aerodigestive tract is common. Oral burns are common and may cause drooling. A lack of oral burns does not exclude esophageal injury. The overall rate of esophageal injury for alkali ingestions is 30%÷40%; such injury is suggested by vomiting, drooling, or stridor.
Esophageal perforation may occur and result in mediastinitis. Esophageal stricture may develop as a late complication.
Gastric injury and perforation also may occur and are much more likely with liquid lye ingestions, as the lye passes rapidly into the stomach.
Crystalline lye ingestion may lead to severe upper airway injury with stridor and airway obstruction that necessitate rapid intervention.
Other symptoms of alkaline ingestion include oral pain, odynophagia, chest pain, abdominal pain, nausea, and vomiting.
Obtain chest and abdominal radiographs for evidence of perforation (pneumomediastinum, pleural effusion, and pneumoperitoneum).
Laboratory Studies
Obtain CBC, electrolytes, BUN, creatinine, and coagulation parameters.
If there are signs suggesting severe burns or perforation, type and cross-match blood.
Immediately rinse the oral cavity copiously with cold water.
Do not induce emesis because it may increase injury.
Charcoal administration, cathartic administration, and gastric lavage are not indicated. Administration of charcoal obscures anatomic detail for subsequent endoscopy.
Diluents are controversial and may induce emesis. Poisindex52 currently recommends administration of diluents (no more than 8 oz milk or water), although other experts strongly disagree, and an update on the Poisindex consensus has not been reported since 1988.
Do not attempt to neutralize the alkaline agent with a weak acid, as this results in an exothermic reaction and increases tissue damage.
Protect the airway and administer oxygen. Endotracheal intubation or early trach- eostomy may be required.
Avoid use of a nasogastric tube.
Establish an IV line and give fluids guided by vital signs.
Monitor the cardiac rhythm and oximetry.
Glucocorticoid treatment of esophageal burns in an attempt to prevent stricture is controversial and generally not recommended.
Prophylactic antibiotics are not appropriate.
If the patient exhibits drooling, stridor, or odynophagia, consult a gastroenterologist to arrange for immediate endoscopy; otherwise, it can be deferred 12÷24 hours.
Obtain surgical consultation.
Disposition will depend on the results of the evaluation above.
Obtain a barium swallow after 2÷4 weeks to assess for esophageal stricture.
General Principles
Common household acids include most toilet bowl cleaners, drain cleaners, metal cleaners, battery acid, and swimming pool cleaners.
Tissue injury is generally less deep than that produced by alkaline agents.
Gastric and esophageal injuries including perforation are common. Pyloric stricture may result.
Symptoms include oral pain, drooling, odynophagia, and abdominal pain.
Severe cases may have respiratory distress, DIC, hemolysis, and systemic acidosis.
Obtain an upright chest radiograph to detect perforation.
Laboratory Studies
Obtain CBC, prothrombin time, partial thromboplastin time, platelet count, electrolytes, BUN, and creatinine.
In severe burns, type and cross-match.
Wash mouth out copiously with cold water.
Diluent administration often is recommended (with the same caveats as noted above for alkaline ingestions) but has no demonstrated clinical efficacy.
Neutralization with a weak base is contraindicated.
Induction of emesis, gastric lavage, and charcoal administration are all contraindicated, and a nasogastric tube should be avoided.
Establish IV access and administer fluids guided by vital signs.
Sucralfate (1 g q6h) may decrease symptoms but does not appear to decrease complications or perforation.
The administration of glucocorticoids is controversial, but their use probably is of no added benefit. Prophylactic antibiotics are not recommended.
Unsuspected esophageal and gastric burns and duodenal injury are commonly seen with endoscopy, which should be performed by a GI consultant within 24 hours. The likelihood of stricture formation (pyloric or esophageal) and perforation depends on the severity of ingestion.
Obtain surgical consultation.
Obtain upper GI radiograph after 2÷4 weeks.
Ethanol and other alcohols
Ethanol (EtOH)
General Principles
The toxicity of ethanol (EtOH) is dose related, but tolerance varies widely.
Blood levels >100 mg/dL are associated with ataxia.
At 200 mg/dL, patients are drowsy and confused.
At levels >400 mg/dL, respiratory depression is common and death is possible.
Laboratory Studies
Obtain electrolytes, glucose level, serum osmolality, and blood EtOH level.
The blood EtOH level can be rapidly estimated by calculating the osmolal gap (measured osmolality minus calculated osmolality, or measured osmolality minus [2 Na (mEq/L) + (urea [mg/dL])/2.8 + (glucose [mg/dL])/18]). The standard formula for blood EtOH level in mg/dL equals 4.6 times the osmolal gap,53 in the absence of other low molecular weight toxins. However, multipliers ranging from 2.754 to 3.755 have been reported using linear regression from actual in vivo measurements in humans; thus, if the standard multiplier is used, the patient may appear to have a residual osmolal gap, implying the presence of another toxin such as methanol (MeOH) or ethylene glycol (EG) when there is none.
If the patient's mental status is severely depressed, insert an endotracheal tube before performing gastric lavage if the patient presents <1 hour after ingestion.
Charcoal is not helpful due to the rapid absorption of EtOH from the stomach.
Hemodialysis may be useful for life-threatening overdoses.
Administer 100 mg thiamine IV followed by 50 mL 50% dextrose in water IV to any comatose alcoholic patient.
Admit patients with alcohol intoxication if they have severe underlying illness or significant alcoholic ketoacidosis or if ventilatory support is required.
Observe other patients until they are sober (blood alcohol level <100 mg/dL) or can be discharged to the care of a responsible sober adult.
If the patient's mental status is more abnormal than would be expected for the blood alcohol level, consider additional toxicology testing and head CT.
Isopropyl Alcohol
General Principles
Most rubbing alcohol is 70% isopropyl alcohol (IPA). IPA is more toxic than EtOH at any blood level (50 mg/dL = intoxication, 100÷200 mg/dL = stupor and coma). Respiratory depression and hypotension occur at high blood levels.
Other symptoms include nausea, vomiting, and abdominal pain.
Workup commonly reveals ketosis without acidosis (IPA is metabolized to acetone).
Metabolic acidosis, if present, is usually related to associated hypotension.
IPA concentration in the blood can be measured directly or can be estimated in the same fashion as for EtOH, substituting a multiplier of 6.0 for 4.6. Absence of an osmolal gap
does not exclude IPA ingestion. Measure plasma glucose, as hypoglycemia may occur, particularly in children.
If diagnosis is in doubt, obtain blood levels of other toxic alcohols and determine acid-base status with ABGs.
Do not induce emesis, as mental status may decline rapidly, with subsequent aspiration.
Gastric lavage followed by charcoal administration may be useful if performed within 60 minutes of ingestion. Protect the airway.
For cutaneous exposures, wash the skin and remove contaminated clothes. Maintain an adequate airway and support BP.
Hemodialysis is reserved for patients with persistent hypotension despite supportive therapy.
General Principles
Methanol (MeOH) is in gas-line antifreeze, carburetor fluid, duplicator fluid, and windshield washer fluid.
Sterno Canned Heat fuel contains EtOH and MeOH, and the EtOH that is present may delay manifestations of MeOH toxicity.
The toxicity of MeOH is due to its conversion by alcohol dehydrogenase to formaldehyde and then by acetaldehyde dehydrogenase to formic acid. Initial symptoms may include lethargy and confusion, followed by an apparent hangover.
Clinical Presentation
MeOH toxicity presents with headache, visual symptoms (blurring, diminished acuity, and whiteness in the visual field), nausea, vomiting, abdominal pain, tachypnea, and respiratory failure.
Coma and convulsions may occur in severe MeOH intoxication. The range of toxic ingestion is 15÷400 mL
Symptoms may be delayed 18÷24 hours.
Physical Examination
Typically, examination reveals an uncomfortable patient who may be remarkably tachy- pneic with decreased visual acuity; optic disk hyperemia may be hard to appreciate.
Laboratory Studies
Obtain CBC, electrolytes, BUN, creatinine, amylase, urinalysis, EtOH, and MeOH levels, as well as ABGs, which reveal a severe anion-gap metabolic acidosis. Development of the acidosis may be delayed 18 hours or more, until the accumulation of toxic metabolites; coingestion of alcohol may prolong this phase for many hours.
In general, pH and acid-base status are better predictors of toxicity than is the absolute MeOH level.
The MeOH level (in mg/dL) can be estimated in the same way as for EtOH, substituting a multiplier of 3.2 for 4.6. However, the absence of an osmolal gap does not rule out MeOH intoxication, and for the reasons noted above, EtOH intoxication may result in an apparent osmolal gap that is greater than anticipated, leading to temporary misdiagnosis of intoxication with MeOH or another osmotically active toxin.
Do not induce emesis.
Consider gastric lavage if the patient is seen <1 hour after ingestion. Charcoal does not absorb significant amounts of MeOH.
Give folinic acid (leucovorin), 1 mg/kg (maximum, 50 mg) IV, followed by folic acid, 1 mg/kg IV q4h for six doses, to increase the metabolism of formate.
Administering IV NaHCO3 for severe acidosis may reduce permanent vision damage.
4-Methylpyrazole (fomepizole; an alcohol dehydrogenase antagonist)56 is FDA approved for the treatment of MeOH toxicity, although no direct comparison with EtOH has been made. Nevertheless, it is more easily administered than EtOH and does not cause depression of mental status or hypoglycemia. Although much more expensive, it is now the antidote of choice.
In the United States, emergency orders may be placed with Jazz Pharmaceuticals, (800) 359÷4304.
Administer fomepizole for the following indications: peak MeOH level >20 mg/dL, while awaiting levels for an ingestion suspected of being MeOH, or an anion-gap metabolic acidosis after suspicious ingestion.
The dosage is 15 mg/kg IV followed by 10 mg/kg IV q12h for four doses. This should be followed by 15 mg/kg IV q12h until the MeOH level is <20 mg/dL. During hemodialysis, the dosing interval should be changed to q4h (Table 25-3).
EtOH delays metabolism of MeOH to its toxic metabolites by competing for alcohol dehydrogenase and can be used in situations in which fomepizole is unavailable or contraindicated.
Administer EtOH for the following indications: peak MeOH level >20 mg/dL, while awaiting levels for an ingestion suspected of being MeOH, or an anion-gap metabolic acidosis after suspicious ingestion.
The loading dose of EtOH is 7.6÷10 mL/kg of a 10% solution, given IV, or 0.8÷1 mL/kg of 95% alcohol, administered PO in orange juice. EtOH for infusion is available as stock 5% or 10% solutions in D5W; the latter is preferred. EtOH (10%) for IV infusion can also be prepared by removing 100 mL D5W from a 1-L bag and replacing it with 100 mL absolute alcohol. Maintenance dosage varies depending on previous alcohol exposure (Table 25-4).
The goal is achievement of a blood alcohol level of 100÷130 mg/dL to saturate the available alcohol dehydrogenase and prevent formation of MeOH's toxic metabolites. Check EtOH levels 1 hour after the loading dose and at least two to three times a day during maintenance infusion (some authorities recommend hourly levels). It is ultimately less hazardous to the patient to have blood alcohol levels that are too high than too low. Monitor blood glucose levels, as hypoglycemia may occur. Administer EtOH continuously until the MeOH level is <10 mg/dL, the formate level is <1.2 mg/dL, there is resolution of acidosis, CNS symptoms abate, and a normal anion gap is restored.
This implies regular monitoring of electrolytes, BUN, creatinine, and ABGs. If MeOH levels cannot be readily measured, administer EtOH for at least 9 days without dialysis (or 1 day with dialysis) and until clinical findings resolve.57 Every effort should be made to move the patient to a center where levels and dialysis are available.
Special Therapy
Hemodialysis generally is indicated for an MeOH level that exceeds 50 mg/dL, severe and resistant acidosis, renal failure, or visual symptoms. Adjust fomepizole and ethanol doses as shown in Tables 25-3 and 25-4.
Ethylene Glycol and Diethylene Glycol
General Principles
Ethylene glycol is used commonly in antifreeze and windshield deicer. Various metabolites are responsible for toxicity.
Clinical Presentation
The initial syndrome resembles alcohol intoxication.
Vomiting is common.
CNS depression, seizures, or coma may occur.
CHF and pulmonary edema may occur 12÷36 hours after ingestion. Death is most likely in this stage.
Oliguric renal failure (from oxalate crystal deposition) may occur 24÷72 hours after ingestion. Associated flank pain may be prominent.
Laboratory Studies
Obtain electrolyte, BUN, and creatinine levels; serum osmolality; ABGs; urinalysis; and EtOH and EG levels.
Findings include a severe metabolic acidosis with an anion gap (which may be delayed for hours until accumulation of toxic metabolites occurs), an osmolal gap, and oxalate and hippurate crystalluria in addition to hematuria and proteinuria.
Serum level can be calculated from the osmolal gap as for EtOH, using a multiplier of 6.2.
Fluorescein often is added to antifreeze, and urine fluorescence detected with a Wood lamp up to 6 hours after ingestion is diagnostic,58 although the accuracy of this has been disputed.59
Do not induce emesis.
Neither gastric lavage nor charcoal administration is likely to be effective but can be considered if the patient presents within 1 hour of ingestion, particularly if the ingestion is mixed with other toxins that are amenable to gastric decontamination.
Avoid magnesium salt cathartics because of the likelihood of renal failure.
Correct life-threatening acidosis with IV sodium bicarbonate pending dialysis; administration for lesser severity is not justified. Administer 1÷3 mEq/kg IV and titrate to achieve a normal pH. Monitor the calcium level, as hypocalcemia may result.
4-Methylpyrazole (fomepizole)60,61 is FDA approved for use in EG poisoning. Indications include an EG level >20 mg/dL, a suspected EG ingestion (while levels are being awaited), or an anion-gap metabolic acidosis with a history of EG ingestion, regardless of level. The dosing is similar to the treatment of MeOH poisoning. Treatment with 4-methylpyrazole should continue until the EG level is <20 mg/dL.62
IV EtOH (although not FDA approved and never studied prospectively; Table 25-4) can be used as an alternative when fomepizole is unavailable or contraindicated (hypersensitivity). It is dosed in the same manner as for MeOH intoxication. It should be continued until the EG level is <10 mg/dL, with no symptoms and a normal pH. An EtOH level of at least 100 mg/dL should be maintained. If levels are unavailable, infusion should be continued for at least 3 days, or 1 day with dialysis. Every effort should be made to transfer the patient safely to a facility with the capacity to measure EG levels and perform dialysis.
Administer pyridoxine (100 mg IV daily) to promote the conversion of glyoxylate to glycine and thiamine (100 mg IV daily) to promote the formation of nontoxic α-hydroxy-beta-ketoadipic acid.
Special Therapy
Dialysis is highly effective in severe cases. Fomepizole dosage is adjusted as in Table 25-3. EtOH infusion should be continued at higher doses (Table 25-4) during dialysis.
Indications are glycol level >50 mg/dL (unless the patient is being given 4-methylpyrazole and the patient is asymptomatic with a normal pH), electrolyte abnormalities that are unresponsive to standard therapy, deteriorating vital signs despite supportive therapy, renal failure, or a pH of <7.25÷7.30 that is unresponsive to therapy.62
Discontinue when the glycol level is <10 mg/dL, the glycolic acid level is undetectable, and the acidosis, clinical status, and anion gap have returned to normal.
When levels cannot be measured easily, continue EtOH administration for at least 3 days without hemodialysis (or for 1 day with hemodialysis) and until clinical findings resolve, whichever is longer.63 Measure EtOH levels after the loading dose and two to three times a day during maintenance therapy.
General Principles
Morbidity and mortality usually are attributed to pulmonary aspiration. Low viscosity (e.g., kerosene, gasoline, and liquid furniture polish) is associated with greater aspiration potential. Motor oil, transmission oil, mineral oil, baby oil, and suntan oil usually are nontoxic.
Clinical Presentation
Hydrocarbon ingestions are characterized by GI upset, pulmonary aspiration, and CNS alterations.
Clinical manifestations usually are apparent within the first 6 hours and include vomiting, chest or abdominal pain, cough, dyspnea, low-grade fever, arrhythmias, an altered sensorium, seizures, and radiographic evidence of aspiration pneumonitis or pulmonary edema.
Obtain a chest radiograph.
Treatment of nontoxic hydrocarbon ingestion is not required in the absence of symptoms. These agents have high aspiration potential but are associated with little or no GI absorption. Gastric emptying is never necessary.
Treatment of toxic hydrocarbon ingestion is begun by removing contaminated clothing and washing the affected skin to prevent dermatitis and percutaneous absorption.
Provide supplemental oxygen to patients with significant aspiration injuries.
Gastric emptying, although controversial, is recommended for ingestion of toxic hydrocarbons, particularly halogenated hydrocarbons (trichloroethylene, carbon tetrachloride, methylene chloride) or those that contain toxic additives (e.g., heavy metals, insecticides, nitrobenzene, aniline, or camphor), although some authorities recommend only administration of activated charcoal. Other potentially toxic hydrocarbons (gasoline, benzene, kerosene, lighter fluid, paint thinner, and toluene), except for large suicidal ingestions, do not require gastric emptying.
If gastric emptying is performed, this is one of the few potential indications for ipecac, as aspiration appears to be less frequent with the use of ipecac than after gastric lavage. Therefore, in alert patients with a very strong indication, consider inducing emesis with ipecac, 30 mL PO. Perform gastric lavage after intubation with a cuffed endotracheal tube in any patient with CNS depression, a depressed gag reflex, or seizures.
Prophylactic antibiotics or glucocorticoids are not indicated.
Observe the patient for at least 6 hours after gastric decontamination.
Hospitalize patients who are lethargic or have pulmonary symptoms or an abnormal pulmonary examination, ABGs, or chest radiograph.
Patients who remain asymptomatic with a normal chest radiograph after 6 hours may be discharged.
General Principles
Lithium is administered as a carbonate or citrate salt for the treatment of psychiatric disease, principally bipolar disorder. Overdose often is suicidal.
Excretion is renal. States of dehydration and sodium uptake promote lithium retention and toxicity, as does thiazide diuretic use.
Symptoms are loosely related to blood level in acute overdose. Therapeutic blood levels range between 0.6 and 1.2 mEq/L.
At <2.5 mEq/L, symptoms are mild and consist of tremor, ataxia, nystagmus, and lethargy.
Between 2.5 and 3.5 mEq/L, the patient may be agitated and confused and have fasciculations, nausea, vomiting, and diarrhea.
Levels >3.5 mEq/L are associated with seizures, coma, cardiac arrhythmias, hypotension, noncardiogenic pulmonary edema, nephrogenic diabetes insipidus, and death. Levels associated with severe symptoms may be lower in those with chronic ingestion.
Laboratory Studies
Obtain electrolytes, creatinine, and lithium level.
Electrolytes may reveal a low anion gap with elevated bicarbonate, and there may be evidence of diabetes insipidus.
Lithium levels should be measured repetitively until at least two sequential levels show continued decline.
Obtain an ECG and monitor the patient continuously while he or she is being evaluated and treated.
Consider gastric lavage if the patient presents within 1 hour of ingestion.
Charcoal does not bind lithium; sodium polystyrene sulfonate (15 g PO qid or 30÷50 g per rectum) can decrease absorption.64
Sustained-release preparations may form concretions. If levels continue to rise despite treatment, perform whole-bowel irrigation with commercial polyethylene glycol solution, 2 L/hr for 5 hours.
Establish IV access and hydrate with 0.9% saline to achieve euvolemia. Avoid dehydration, as this promotes renal lithium reabsorption.
Treat arrhythmias in standard fashion (see Chapter 7, Cardiac Arrhythmias).
Criteria for dialysis are inexact. Consult a nephrologist for consideration of hemodialysis (preferably with a bicarbonate rather than acetate bath) for the following indications: blood level >3.5÷4.0 mEq/L after an acute ingestion, chronic toxicity with a blood level >2.5 mEq/L, worsening mental status, seizures, dysrhythmias, pulmonary edema, and renal failure.
The goal is achievement of a sustained level of 1 mEq/L 8 hours after dialysis, which may necessitate prolonged or repeated dialysis.
Methemoglobinemia (acquired)
General Principles
Methemoglobinemia can be caused by nitrites, nitroprusside, nitroglycerin, chlorates, sulfonamides, aniline dyes, nitrobenzene, antimalarials, and phenazopyridine.
Methemoglobinemia has also been reported after benzocaine topical anesthesia for endoscopy as well as other topical anesthetics65 and after dapsone therapy.66
Symptoms include headache, fatigue, lethargy, dyspnea, tachycardia, and dizziness. The patient may be hypotensive due to the vasodilating properties of nitrates as well as tissue hypoxia. Seizures may occur.
Severity correlates with methemoglobin level. Blood levels exceeding 50% indicate severe toxicity, often associated with CNS depression, seizures, coma, and arrhythmias; levels higher than 70% are often fatal.
Obtain CBC, electrolytes, ABGs, and methemoglobin level.
The diagnosis is suggested in patients with a normal oxygen tension (as measured by ABGs) and generalized cyanosis (corresponding to a methemoglobin level of 15% or more) that does not respond to oxygen.
Blood with that level of methemoglobin placed on white filter paper appears chocolate colored when exposed to room air as compared to blood from a normal control.
Measured arterial oxygen saturation that is much lower than that calculated for the alveolar oxygen tension also is suspicious for methemoglobinemia.
Obtain an ECG and monitor the cardiac rhythm continuously.
Give 100% oxygen.
Do not give ipecac because seizures may occur and promote aspiration.
Consider gastric lavage (with airway protection) if the patient presents within 1 hour of ingestion or has coma or seizures.
Administer activated charcoal.
If signs of hypoxia are present or if the methemoglobin level exceeds 30%, administer methylene blue, 1÷2 mg/kg in a 1% solution IV over 5 minutes.
The dose can be repeated in 1 hour if signs of hypoxia persist and q4h thereafter to a maximum dose of 7 mg/kg.
Treat seizures with a benzodiazepine and phenytoin in addition to methylene blue.
Treat hypotension with IV fluids and, if resistant, with dopamine.
Hyperbaric oxygen and exchange transfusion are extreme measures for severely symptomatic patients.
Hospitalize the patient in an ICU if he or she is symptomatic or if the methemoglobin level is >20%.
Symptoms of opioid overdose are respiratory depression, a depressed level of consciousness, and miosis. However, the pupils may be dilated with acidosis or hypoxia
or after overdoses with meperidine or diphenoxylate plus atropine. Overdose with α-methylfentanyl (“China white”) may result in negative toxicology screens.
Special Considerations
Heroin may be adulterated with scopolamine, cocaine, or caffeine, complicating the clinical picture. Less common complications include hypotension, bradycardia, and pulmonary edema.
Be aware of body packers, who smuggle heroin in their intestinal tracts. Deterioration of latex or plastic containers may result in drug release and death.70
Laboratory Studies
Drug levels and other standard laboratory tests are of little use. Pulse oximetry and ABGs are useful for monitoring respiratory status.
Chest radiograph should be obtained if pulmonary symptoms are present.
Treatment includes airway maintenance, ventilatory and circulatory support, and prevention of further drug absorption.
Emesis is contraindicated.
Gastric lavage can be considered for oral ingestions that present within 1 hour; administer activated charcoal.
Whole-bowel irrigation may be safe and effective for body packers; surgery is not indicated except for obstruction. Endoscopic removal should not be attempted due to the danger of rupture.
Naloxone hydrochloride specifically reverses opioid-induced respiratory and CNS depression and hypotension. The initial dose is 2 mg IV; large doses may be required to reverse the effects of propoxyphene, diphenoxylate, buprenorphine, or pentazocine.
In the absence of an IV line, naloxone can be administered sublingually,67 via endotra-cheal tube, or intranasally.68 Isolated opioid overdose is unlikely if there is no response to a total of 10 mg naloxone. Repetitive doses may be required (duration of action is 45 minutes), and this should prompt hospitalization despite the patient's return to an alert status.
Methadone overdose may require therapy for 24÷48 hours, whereas levo-α-acetylmethadol may require therapy for 72 hours. A continuous IV drip that provides two-thirds of the initial dose of naloxone hourly, diluted in D5W, may be necessary to maintain an alert state.69
Ventilatory support should be provided for the patient who is unresponsive to naloxone and for pulmonary edema.
If the patient is alert and asymptomatic for 6 hours after an oral ingestion and a single dose of naloxone, or for 4 hours after a single treatment for an IV overdose, he or she can be discharged safely.
Body packers should be admitted to an ICU for close monitoring of the respiratory rate and level of consciousness and remain so until all packets have passed, as documented by CT.
General Principles
Organophosphates are responsible for a number of human poisonings, particularly in developing countries. Parathion and malathion are the most common insecticides involved; they often are contained in hydrocarbon solvent.
Suicidal ingestion and agricultural exposure, including dermal absorption, occur. “Nerve gases” used in terrorist biowarfare are anticholinesterases, such as sarin.
Toxic manifestations are due to inhibition of acetylcholinesterase in the nervous system.
Muscarinic manifestations include miosis, increased lacrimation, blurred vision, bronchospasm, bronchorrhea, diaphoresis, salivation, bradycardia, urinary incontinence, and increased GI motility, manifested by cramps, nausea, vomiting, and diarrhea.
Among the nicotinic manifestations are muscle weakness and cramps, muscle fasciculations, hypotension, and respiratory paralysis.
CNS toxicity is characterized by anxiety, slurred speech, mental status changes (e.g., delirium, coma, and seizures), and respiratory depression.
Complications of ingestion include pulmonary edema, aspiration pneumonia, chemical pneumonitis, delayed polyneuropathy, and ARDS.
Nonketotic hyperglycemia and glucosuria are common.
Hyperamylasemia may reflect pancreatitis.
Red cell cholinesterase and plasma pseudocholinesterase levels are decreased; activities of <50% of baseline are associated with poor outcome.
Laboratory Studies
Obtain CBC, electrolytes, ABGs, and plasma and red cell cholinesterase levels.
Obtain chest radiograph and ECG.
Monitor ABGs and ECG; QTc prolongation is associated with a worse prognosis.
Apply measures to support ventilation and circulation, decontaminate the skin (the medical team should wear rubber gloves, aprons, and shoe covers if there is major skin contamination), and consider gastric lavage for oral poisonings if presentation is within 1 hour of ingestion; induction of emesis is contraindicated.
Administer activated charcoal.
Atropine (preservative free, to avoid benzyl alcohol toxicity with large doses) is the drug of choice for organophosphate toxicity.
Give an initial dose of 1 mg IV; if the patient experiences no adverse effects, repeat a dose of 2 mg q15min until atropinization (as manifested by drying of secretions, tachycardia, flushing, dry mouth, and dilated pupils) occurs.
The average patient requires approximately 40 mg/d, but larger doses (500÷1,500 mg/d) may be necessary. Intermittent administration may have to be continued for at least 24 hours until the organophosphate is metabolized.
Severe cases may require several days or more of therapy, because of slow regeneration of acetylcholinesterase activity. Atropine does not reverse the muscle weakness.
Give pralidoxime, 1÷2 g IV in 100 mL normal saline over 30 minutes, which reactivates the cholinesterase and counteracts weakness, muscle fasciculations, and respiratory depression. Repeat administration q6÷12h to a maximum of 12 g in 24 hours. An alternative is continuous infusion at 500 mg/hr as needed for several days. Unlike organophosphates, carbamate intoxications do not irreversibly inhibit cholinesterase, and thus pralidoxime is not usually required and may worsen symptoms.
Treat seizures with a benzodiazepine and phenytoin; if severe seizures require muscle relaxants, do not use succinylcholine, which may result in prolonged paralysis.
Hemoperfusion should be considered for severe parathion overdoses, although there is little objective evidence to support its use.
Support respiratory failure with mechanical ventilation.
General Principles
Phencyclidine is a dissociative anesthetic and is available illicitly, mislabeled as LSD, mescaline, psilocybin, and tetrahydrocannabinol. Frequency of use varies widely by geographic region and is frequent in some urban areas but uncommon in many other parts of the United States.
Symptoms that occur even with small ingestions include agitation, hallucinations, bizarre or violent behavior, hypertension, tachycardia, and horizontal or vertical nystagmus.
Patients are relatively impervious to pain and may be catatonic or self-destructive and difficult to subdue.
Stupor progressing to coma, hypertension, hyperpyrexia, hypertonicity, and bronchospasm characterizes moderate ingestions.
Massive ingestions may lead to hypotension, respiratory failure, rhabdomyolysis, and acute tubular necrosis. Hypoglycemia is common, and death may occur.
Laboratory Studies
Monitor electrolytes, creatinine, and creatine phosphokinase (CPK). Drug levels are not useful.
Treatment is primarily supportive.
Minimize sensory input and remove potentially injurious objects from the area.
Ipecac is contraindicated.
Gastric lavage may provoke violent behavior and is recommended only in severe poisonings and only after the airway has been protected.
Repeated charcoal administration also may interrupt enterogastric and enterohepatic circulations but has not been demonstrated to have an effect on outcome.
Use diazepam to control agitation; give haloperidol if the agitation is severe.
Treat dystonic reactions with diphenhydramine.
Control adrenergic manifestations (e.g., hypertension) with β-adrenergic blockade if bronchospasm is not present; sodium nitroprusside may be required in severe cases.
Seizures are uncommon in adults; treat with benzodiazepines and phenytoin. Consider discharging any patient with low-dose intoxication from the emergency department after his or her symptoms resolve and psychiatric consultation has been obtained. Hospitalize patients with more severe intoxication.
Acid diuresis is no longer recommended.
Avoid restraints, as they may increase rhabdomyolysis.
Treat hyperthermia with cooling and hydration.
Consider discharge after low-dose ingestion after symptoms resolve and psychiatric consultation has been obtained.
Hospitalize those with more severe overdose.
General Principles
Neuroleptics are antipsychotics.
Phenothiazines that are used commonly include chlorpromazine, thioridazine, prochlorperazine, perphenazine, trifluoperazine, fluphenazine, mesoridazine, haloperidol (a butyrophenone), and thiothixene.
Clinical Presentation
Overdoses are characterized by agitation or delirium, which may progress rapidly to coma. Pupils may be mydriatic and deep tendon reflexes are depressed. Seizures and disorders of thermoregulation, particularly hyperthermia, may occur.
Hypotension (due to strong α-adrenergic antagonism), tachycardia, arrhythmias (including torsades de pointes), and depressed cardiac conduction occur.
Laboratory Studies
Measuring blood levels is not helpful.
Radiographs may reveal pill concretions that are present in the stomach despite apparently effective gastric emptying.
Monitor the cardiac rhythm continuously.
Treatment includes airway protection, respiratory and hemodynamic support, and administration of activated charcoal.
Emesis is contraindicated.
Consider gastric lavage, which may be effective hours later due to delayed gastric emptying caused by the phenothiazines.
Consider whole-bowel irrigation for ingestion of sustained-release formulations.
Monitor the cardiac rhythm.
Treat ventricular arrhythmias with lidocaine and phenytoin; class Ia agents (e.g., procainamide, quinidine, disopyramide) are contraindicated; avoid sotalol.
Treat hypotension with IV fluid administration and α-adrenergic vasopressors (nor- epinephrine). Dopamine is an acceptable alternative. Paradoxic vasodilation may occur in response to epinephrine administration because of unopposed β-adrenergic response in the setting of strong α-adrenergic antagonism.
Recurrent torsades de pointes may require magnesium, isoproterenol, or overdrive pacing (see Chapter 7, Cardiac Arrhythmias).
Treat seizures with diazepam and phenytoin.
Treat dystonic reactions with benztropine, 1÷4 mg, or diphenhydramine, 25÷50 mg, IM or IV.
Treat hyperthermia with cooling. Forced diuresis, hemodialysis, and hemoperfusion are not useful.
Frank neuroleptic malignant syndrome may complicate use of these agents, and should be treated as described above.
Admit those patients who have ingested a significant overdose for cardiac monitoring for at least 48 hours.
Atypical neuroleptics
Clinical Presentation
Overdose is characterized by altered mental status, ranging from somnolence to coma. Anticholinergic effects occur, including blurred vision, dry mouth (although hypersalivation may occur in overdose), lethargy, delirium, and constipation. Seizures occur in a minority of overdoses. Coma may occur.
Physical manifestations include hypotension, tachycardia, fasciculations, tremor, and myoclonus. Agranulocytosis may result. ECG abnormalities are unusual, but atrioventricular block may occur. Serious dysrhythmias rarely occur.
Laboratory Studies
Obtain WBC and liver function tests; follow the WBC weekly for 4 weeks. Clozapine levels are not useful.
Induction of emesis is contraindicated.
Perform gastric lavage if the patient presents within 1 hour of ingestion.
Give activated charcoal.
Treat hypotension with crystalloids; if resistant, treat with norepinephrine or dopamine.
Treat seizures with benzodiazepines and phenytoin.
Provide ventilatory support for respiratory failure.
No evidence has been shown that forced diuresis, hemodialysis, or hemoperfusion is beneficial
Filgrastim can be given for agranulocytosis.
Admit and monitor patients with severely symptomatic overdoses for 24 hours or more.
Clinical Presentation
Overdose is characterized by somnolence, slurred speech, ataxia, vertigo, nausea, and vomiting.71
Anticholinergic effects occur, including blurred vision, dry mouth, and tachycardia.
Seizures are uncommon. Coma may occur.
Physical manifestations include hypotension, tachycardia, and pinpoint pupils that are unresponsive to naloxone. Serious dysrhythmias rarely occur.
Induction of emesis is contraindicated.
Consider gastric lavage if presentation is within 1 hour of ingestion.
Give activated charcoal.
Treat hypotension with fluids and, if ineffective, norepinephrine or dopamine.
Give benzodiazepines and phenytoin for seizures.
Provide ventilatory support for respiratory failure, which occurs uncommonly.
Risperidone, ziprasidone, and quetiapine
These agents are newer atypical antipsychotics with limited information about overdose.
Clinical Effects
These include CNS depression, tachycardia, hypotension, and electrolyte abnormalities. QRS and QTc prolongation have occurred with each, but clinically significant ventricular dysrhythmias are uncommon.
Laboratory Studies
Monitor electrolytes, liver function, and ECG with continuous telemetry.
Do not induce emesis.
Consider gastric lavage if presentation is within 1 hour of ingestion.
Administer activated charcoal.
Monitor and provide support for respiratory depression.
Treat hypotension with fluids, and if severe and persistent, norepinephrine in preference to dopamine.
Treat ventricular dysrhythmias with sodium bicarbonate to maintain a pH of 7.45÷7.55, and avoid Ia antiarrhythmics (procainamide, quinidine, and disopyramide).
Diuresis, hemodialysis, and hemoperfusion do not appear to be useful.
General Principles
Salicylate toxicity may result from acute ingestion or chronic intoxication. Toxicity is usually mild after acute ingestions of <150 mg/kg, moderate after ingestions of 150÷300 mg/kg, and generally severe with overdoses of 300÷500 mg/kg.
Toxicity from chronic ingestion typically is due to intake of >100 mg/kg/d over a period of several days and usually occurs in elderly patients with chronic underlying illness. Diagnosis often is delayed in this group of patients, and mortality is approximately
25%. Significant toxicity due to chronic ingestion may occur with blood levels lower than those associated with acute ingestions.
Nausea, vomiting, tinnitus (implying levels >30 mg/dL), hyperpnea, and malaise can occur. Fever suggests a poor prognosis in adults.
Severe intoxications are associated with lethargy, convulsions, and coma, which may result from cerebral edema.
Noncardiogenic pulmonary edema occurs in up to 30% of adults and is more common with chronic ingestion, cigarette smoking, neurologic symptoms, and older age.
Severe overdoses are manifested by tachypnea, dehydration, pulmonary edema, altered mental status, seizures, coma, or a total dose >300 mg/kg.
Laboratory Studies
Obtain CBC, electrolytes, BUN, creatinine blood glucose levels, and prothrombin and partial thromboplastin times. Prothrombin time prolongation is common.
Hypoglycemia, common in children, is rare in adults.
ABGs may reveal an early respiratory alkalosis, followed by metabolic acidosis. Approximately 20% of patients exhibit either respiratory alkalosis or metabolic acidosis alone.72 Most adults with pure salicylate overdose have a primary metabolic acidosis and a primary respiratory alkalosis. After mixed overdoses, respiratory acidosis may become prominent.73
Blood levels must be drawn 6 hours or more after acute ingestion of salicylates to allow prediction of severity of intoxication and patient disposition (Fig. 25-2). Obtaining earlier levels is appropriate in severely intoxicated patients, to guide intervention. Levels >70 mg/dL at any time represent moderate to severe intoxication; levels >100 mg/dL are very serious and often fatal. This information is useful only for acute overdoses; estimation of severity is invalidated by the use of enteric-coated aspirin or chronic ingestion. Bicarbonate levels and pH are more useful than salicylate levels as prognostic indicators in chronic intoxication.
Consider gastric lavage if presentation is within 1 hour of ingestion.
Administer activated charcoal.
Multidose charcoal may be useful in severe overdose74 but is not routinely recommended.
Alkaline diuresis is indicated for salicylate blood levels that are >40 mg/dL.
Administer 88 or 100 mEq (two ampules) sodium bicarbonate in 1,000 mL D5W at a rate of 10÷15 mL/kg/hr if the patient is clinically volume depleted until urine flow is achieved.
Maintain alkalinization using the same solution at 2÷3 mL/kg/hr, and monitor urine output, urine pH (target pH, 7÷8), and serum potassium. Achievement of alkaline diuresis often requires the simultaneous administration of at least 20 mEq/L potassium chloride.
Because there is little evidence of improved outcome with alkaline diuresis, and because older patients may have cardiac, renal, and pulmonary comorbidity, avoid vigorous fluid therapy in the elderly, as pulmonary edema is more likely to occur in this population.
Although acetazolamide causes urine alkalinization, the associated acidemia increases salicylate toxicity, and therefore it must not be used.
Treat cerebral edema with hyperventilation and osmotic diuresis.
Figure 25-2 Severity of salicylate intoxication. (Adapted from
Done AK. Salicylate intoxication. Pediatrics 1960;26:800.
 Treat seizures with a benzodiazepine (diazepam, 5÷10 mg IV q15min up to 50 mg) followed by phenobarbital, 15 mg/kg IV.
Hemodialysis is indicated for blood levels >100÷130 mg/dL after acute intoxication but may be useful with chronic toxicity when levels are as low as 40 mg/dL if other indications for dialysis exist. Among these are refractory acidosis, severe CNS symptoms, progressive clinical deterioration, pulmonary edema, and renal failure.
Treatment of pulmonary edema may also require mechanical ventilation with a high fraction of inspired oxygen concentration and PEEP.
The elderly are at high risk. Repeated blood levels that fail to decline should prompt contrast radiography of the stomach; concretions should be subjected to bicarbonate lavage and multidose charcoal, and whole-bowel irrigation should be considered.
Patients with minor symptoms (nausea, vomiting, tinnitus), an acute ingestion of <150 mg/kg, and a first blood level of <65 mg/dL can be treated in the emergency department. Blood levels should be repeated q2h until they show a decline. These patients often
are medically stable for discharge, and their disposition can be determined based on psychiatric evaluation.
Admit moderately symptomatic patients for at least 24 hours.
Admit patients with severe overdoses to an ICU.
General Principles
Toxic manifestations of barbiturates vary with the amount of ingestion, type of drug, and length of time since ingestion.
Toxicity can occur with lower doses of the short-acting barbiturates (e.g., butabarbital, hexobarbital, secobarbital, and pentobarbital) than of the long-acting barbiturates (e.g., phenobarbital, barbital, mephobarbital, and primidone), but fatalities are more common with the latter.
Clinical Presentation
Mild intoxication resembles alcohol intoxication. Moderate intoxication is characterized by greater depression of mental status, response only to painful stimuli, decreased deep tendon reflexes, and slow respirations. Severe intoxication causes coma and a loss of all reflexes (except the pupillary light reflex).
Plantar reflexes are extensor. Characteristic bullae (“barb burns”) may be seen over pressure points and on the dorsum of the fingers.75 Hypothermia and hypotension may occur. In severe cases, no electrical activity is seen on an EEG.
Maintain a patent airway and adequate ventilation.
Do not induce emesis.
Perform gastric lavage if presentation occurs within 1 hour of ingestion.
Administer multidose activated charcoal. Multidose activated charcoal markedly decreases the half-life of phenobarbital.
Forced alkaline diuresis, similar to that used for salicylate intoxication, is effective in enhancing phenobarbital excretion, but not that of short-acting barbiturates. Its use should be reserved for severe, life-threatening intoxication.
Hemoperfusion may be effective for excretion of phenobarbital and short-acting barbiturates. Hemoperfusion is used rather than hemodialysis because of better drug removal but is reserved for patients with stage IV coma with increased blood levels and refractory hemodynamic compromise.
Treat hypotension with crystalloid administration. If this fails, administer nor- epinephrine or dopamine.
General Principles
Most overdoses are the result of attempts at self-harm. Fatalities are rare; mixed overdoses are common.
An exception is flunitrazepam (Rohypnol, “roofies”), which is ten times as potent as diazepam. It is mixed with low-quality heroin and used to soften the effects of cocaine. It is also mixed with alcohol as a “date rape” drug. Effects are similar to those of
other benzodiazepines. It may cause hallucinations, and mixing with alcohol increases respiratory depression. It often is not detected on standard toxicology screens.
Symptoms include drowsiness, dysarthria, ataxia, slurred speech, and confusion. Severe overdoses may result in coma and respiratory depression.
Do not induce emesis.
Consider gastric lavage if presentation is within 1 hour of ingestion.
Administer activated charcoal.
Provide general supportive measures for hypotension and bradycardia.
Rarely, respiratory depression may require intubation.
Flumazenil, a benzodiazepine antagonist, reverses toxicity without causing respiratory depression.
Administer 0.2 mg (2 mL) IV over 30 seconds, followed by 0.3 mg at 1-minute intervals to a total dose of 3 mg.
If no response is observed after such treatment, benzodiazepines are unlikely to be the cause of the patient's sedation.
If a partial response has occurred, give additional 0.5-mg increments to a total of 5 mg. Rarely, as much as a 10-mg total dose may be necessary for full reversal. If no IV access is available, the drug can be administered by endotracheal tube.
Treat recurrence of sedation or respiratory depression by repeating the preceding regimen or by continuous infusion of 0.1÷0.5 mg/hr.
If mixed overdose with cyclic antidepressants is suspected or the patient has a known history of seizure disorder, flumazenil should not be used.
Forced diuresis and hemodialysis are ineffective.
General Principles
γ-Hydroxybutyrate (GHB) is an endogenous short-chain fatty acid that occurs naturally in the body; this until recently illegal substance is not detected by standard toxicology screens. It has emerged as an important intoxicant.
It is now available legitimately, under severely controlled circumstances, for the treatment of narcolepsy as Xyrem.®
It is often sold to participants at large dance parties (“raves”) and has been responsible for mass intoxications,76 though use may be decreasing.77 It has also been used as a “date rape” drug. Synonyms include, but are not limited to, “liquid Ecstasy,” “liquid E,” “grievous bodily harm,” “Georgia home boy,” “soap,” “salty water,” and “organic Quaaludes.”
Symptoms include ataxia, nystagmus, somnolence progressing to coma, vomiting, and random clonic movements of the face and extremities.
EEG recording supports the belief that these represent myoclonus and not true seizures. Respiratory depression may progress to apnea.
Absorption is very rapid, and lavage and activated charcoal administration are of little use.
Do not induce emesis.
The drug is not antagonized by naloxone or flumazenil.
Experimental but no clinical evidence has been found to support the administration of physostigmine, and its use is not recommended.
Administer oxygen and protect the airway; monitor oxygenation.
Drug levels are not usually available, and the drug is not detected on routine toxicology screens.
Obtain electrolytes and glucose and establish an IV line.
Stimulation, including endotracheal intubation, may stimulate violently aggressive behavior.
Give atropine for persistent symptomatic bradycardia.
Treat hypotension with IV fluids; pressors are rarely necessary.
Obtain an ECG and monitor the cardiac rhythm continuously.
Intoxication is usually short lived; coma typically lasts for 1÷2 hours, and full recovery often occurs within 8 hours. Stable asymptomatic patients can be discharged after 6 hours of observation. Admit any patient who is still clinically intoxicated after 6 hours.78
Clinical Presentation
Symptoms include hyperactivity, irritability, delirium, hallucinations, psychosis, mydriasis, hyperpyrexia, flushing, diaphoresis, hypertension, arrhythmias, vomiting, and diarrhea.
Less common manifestations include acute renal failure secondary to rhabdomyolysis, seizures, CNS hemorrhage, coma, myocardial infarction, aortic dissection, and circulatory collapse.
Administer activated charcoal.
Induction of emesis is contraindicated, as it may induce seizures.
Perform gastric lavage only for recent large ingestions.
Establish an IV line.
Monitor electrolytes, renal function, and CPK.
Obtain an ECG and monitor the cardiac rhythm.
Treat agitation with diazepam; physical restraints may increase the occurrence of rhabdomyolysis.
Treat hallucinations and psychosis with haloperidol. Droperidol, 2.5÷5.0 mg IV, may be superior to benzodiazepines for sedation.79 However, it may cause QT prolongation and torsades de pointes; therefore, its use should be reserved for severe agitation that is resistant to benzodiazepines, and continuous cardiac monitoring should be used.
Treat severe hypertension with nitroprusside or a β-adrenergic antagonist; phentolamine can also be considered (see Chapter 4, Hypertension).
Diazepam is the initial drug of choice for seizures, followed by phenytoin or phenobarbital.
Arrhythmias usually respond to propranolol or lidocaine.
Monitor core temperature. Hyperthermia may require cooling blankets, evaporative cooling, or paralysis; if unsuccessful, dantrolene or bromocriptine may be useful. Hemodialysis is not clearly effective.
Treat rhabdomyolysis as outlined in Chapter 11, Renal Diseases.
Admit patients with moderate to severe symptoms or with abnormal vital signs.
3-4 Methylenedioxymethamphetamine (MDMA, “Ecstasy”)
MDMA has been a popular drug of abuse associated with “rave” culture. Surveys have shown that nearly 40% of college students have used it at least once.
It is often used in association with prolonged vigorous dancing, causing dehydration and contributing to hyperthermia.
Clinical Presentation
Symptoms include hypertension, tachycardia, dilated pupils, diaphoresis, and trismus.
Severe intoxications may result in hyperthermia, DIC, muscle rigidity, myoclonus, rhabdomyolysis, acute renal failure, and occasionally the syndrome of inappropriate antidiuretic hormone secretion. Supraventricular and ventricular arrhythmias may occur. Initial confusion and agitation may progress to coma and seizures.
Laboratory Studies
Toxicology screens are unreliable. Initiation of therapy is based on presumptive diagnosis according to history and presentation. Monitor electrolytes, BUN, creatinine, liver function tests, CBC, coagulation studies, and CPK.
Therapy at present is based on case reports and reviews.80
Do not induce emesis, as coma and seizures may occur abruptly.
Gastric lavage is useful only if initiated within 1 hour of ingestion.
Administer activated charcoal.
Establish an IV line and maintain hydration.
Treat agitation with benzodiazepines, with preparation to protect the airway and support ventilation.
β-Adrenergic antagonists may be useful in treatment of tachycardia and hypertension. Severe hypertension may require nitroprusside.
Treat seizures with benzodiazepines followed by phenytoin or phenobarbital.
Treat ventricular arrhythmias with lidocaine, phenytoin, or esmolol.
Cool the hyperthermic patient with evaporative cooling; consider dantrolene administration.
Treat rhabdomyolysis supportively (see Chapter 11, Renal Diseases).
Clinical Presentation
Symptoms include short-lived CNS and sympathetic stimulation, hypertension, tachy- pnea, tachycardia, and mydriasis. Depression of the higher nervous centers ensues rapidly and may result in death.
Mortality may also result from drug-induced seizures, subarachnoid hemorrhage, stroke, or direct cardiac effects (e.g., coronary artery spasm, myocardial injury, and precipitation of lethal arrhythmias).81
Myocardial infarction may be precipitated in individuals without underlying heart disease. Rhabdomyolysis may occur, precipitating renal failure.
Pulmonary edema may develop abruptly after an individual smokes the free alkaloid form of cocaine (“free base”) or its heated bicarbonate precipitant (“crack”). Pneumomediastinum may occur after smoking crack and may progress to pneumothorax. Other pulmonary complications include alveolar hemorrhage, obliterative bronchiolitis, hypersensitivity pneumonitis, and asthma.82 Bowel ischemia and necrosis may occur.
Special situations include body packing, in which “mules” swallow multiple cocaine-containing packets, often latex condoms. Rupture of one or more may result in severe symptoms or death. Body stuffers may ingest crack cocaine that is unwrapped or wrapped only in a layer of cellophane, to avoid arrest. Their course is generally benign, presumably due to poor absorption.
Obtain CBC, electrolytes, urinalysis, and CPK.
Urine screen may be useful to confirm the diagnosis; drug levels are not useful.
Obtain an ECG and monitor the cardiac rhythm continuously.
Obtain abdominal radiographs to detect cocaine-containing packets in the intestinal tract of suspected body packers; Gastrografin®-enhanced CT may be more sensitive.
Maintain a patent airway and support respiration and circulation.
Avoid β-adrenergic antagonists in patients with myocardial ischemia or infarction, as they allow unopposed α-adrenergic vasospasm.83
Labetalol may be preferable, and phentolamine may be useful in selected cases.
Myocardial ischemia and infarction should be managed as outlined in Chapter 5, Ischemic Heart Disease.
Nitroglycerin can be used for ischemic pain.
Treat ventricular arrhythmias with lidocaine; β-adrenergic antagonists may be useful in those without myocardial ischemia.
Use benzodiazepines to decrease the stimulatory effect of cocaine and to treat seizures initially. Follow with phenytoin or phenobarbital for longer-term seizure control.
Treat noncoronary manifestations of adrenergic stimulation with labetalol; severe or sustained hypertension may require treatment with nitroprusside.
Treat rhabdomyolysis and hypotension supportively.
Hyperthermia may require a cooling blanket, evaporative cooling, sedation, or paralysis.
Diuresis and dialysis are not useful.
For body packers with retained packets, perform gentle catharsis with charcoal and psyllium; mineral oil may dissolve latex packets and precipitate toxicity.
Admit such patients to an ICU for monitoring, as rupture may be rapidly fatal.
Whole-bowel irrigation and surgery probably are rarely necessary, although they have been recommended; surgery is clearly indicated only for bowel obstruction.
Attempts at endoscopy are contraindicated, as rupture may result.
Obtain repeated radiographs until the packets are no longer visible. With appropriate care, mortality is <1%.
Body stuffers have a generally benign course. Abdominal radiography is almost invariably negative. Nearly three-fourths of patients remain asymptomatic, and most of the rest have only mild to moderate symptoms. Only 4% have severe toxicity, including seizures, dysrhythmias, and death.84,85 Close observation is nevertheless warranted.
General Principles
Nausea and vomiting are the most common symptoms of theophylline toxicity and are associated with serum levels >20 mg/mL.
Moderate toxicity is largely due to relative epinephrine excess and includes tachycardia, arrhythmias, tremors, and agitation.
Severe toxicity is most common at serum levels >90 mg/mL in the acutely intoxicated, usually younger individual.
Severe toxicity results in hallucinations, seizures (which may be refractory to standard therapy), dysrhythmias (including sinus tachycardia, atrial fibrillation, supraventricular tachycardia, and ventricular tachycardia and fibrillation), and hypotension.
Seizures and cardiac toxicity are likely at serum levels >60 mg/mL in the chronically intoxicated and might occur at even lower levels.
Rhabdomyolysis occurs occasionally.86 The severity of intoxication is modified by chronicity, age of the patient, and the presence of comorbid diseases.
Laboratory Studies
Obtain theophylline levels q2h until a plateau is reached. The peak level may be delayed significantly after the ingestion of sustained-release theophylline preparations, with toxic levels persisting 50÷60 hours after ingestion.
Check potassium, electrolyte, glucose, CPK, calcium, and magnesium levels; BUN; and ABGs.
Obtain a baseline ECG and maintain continuous cardiac monitoring.
Acid-base abnormalities include respiratory alkalosis and metabolic acidosis. Hypo- kalemia, hyperglycemia, hypercalcemia, and hypophosphatemia may be present.
Establish an IV line and perform gastric lavage if the patient has taken a potentially life-threatening acute ingestion. Consider lavage also after a large ingestion of a sustained-release preparation, as a bezoar may form.
Avoid the use of ipecac because of the potential for seizures and aspiration.
Administer activated charcoal. Multidose charcoal decreases the half-life of theophylline by 50%, although it has not been clearly shown to improve outcome.
Consider whole-bowel irrigation with polyethylene glycol solution for overdoses with sustained-release preparations and blood levels that continue to rise despite therapy.
Treat severe nausea with metoclopramide, 10÷60 mg IV, or ondansetron, 0.15 mg/kg IV (8÷10 mg in the average individual). Do not use phenothiazines because of their propensity to lower the seizure threshold.
Treat hypotension with IV crystalloids and, if resistant, with dopamine.
Phenobarbital is preferred to phenytoin for seizure prophylaxis in the severely poisoned patient. The treatment of choice for seizures is a benzodiazepine followed by phenobarbital (10 mg/kg loading dose at 50 mg/min, followed by up to a total of 30 mg/kg at a rate of 50 mg/min, followed by 1÷5 mg/kg/d to maintain therapeutic plasma levels). Because of the cardiovascular and respiratory depressant activities of barbiturates, careful management of the airway and cardiovascular status are mandatory. For those patients who are refractory to phenobarbital therapy, obtain anesthesiology consultation for administration of pentobarbital; muscle paralysis and general anesthesia can be considered.
Arrhythmias should be treated as they would be in nonintoxicated patients. β-adrenergic antagonists may be particularly useful but may precipitate bronchospasm in asthmatics. Because of its short half-life, IV esmolol usually is safer.
Hemoperfusion (charcoal or resin) is preferable to hemodialysis because of faster drug removal and is indicated for:
Intractable seizures or life-threatening cardiovascular complications, regardless of drug level.
A theophylline level that approaches or exceeds 100 mg/mL after an acute overdose.
A theophylline level >60 mg/mL in acute intoxication, with increasing symptoms, and a patient who is intolerant of oral charcoal administration.
A theophylline level >60 mg/mL in chronic intoxication without life-threatening symptoms.
A theophylline level >40 mg/mL in a patient with chronic intoxication and CHF, respiratory insufficiency, hepatic failure,87 or age older than 60 years.
Admit patients who have chronic intoxication, acute ingestion of sustained-release formulations, acute ingestions with levels that fail to fall or are rising despite therapy, or worsening symptoms.
Those with levels that are falling to <20 mg/mL and whose symptoms are resolving can be discharged.
Toxic Inhalants
General Principles
Toxic inhalants comprise a variety of noxious gases and particulate matter that are capable of producing local irritation, asphyxiation, and systemic toxicity.
In the management of exposure victims, identification of the offending agent is critical, and the regional poison control center must be contacted for specific therapeutic guidelines.
Irritant Gases
Irritant gases produce cutaneous burns, mucosal irritation, laryngotracheitis, bronchitis, pneumonitis, bronchospasm, and pulmonary edema (which may be delayed up to 24 hours after exposure).
The more water-soluble gases (e.g., chlorine, ammonia, formaldehyde, sulfur dioxide, ozone) primarily produce inflammation of the eyes, throat, and upper respiratory tract, whereas the less soluble gases (e.g., phosgene, nitrogen dioxide) tend to cause more damage to the terminal airways and alveoli. Household exposure may result from inadvertent mixture of bleach (sodium hypochlorite) with toilet bowl cleaner (sulfuric acid), which produces chlorine gas, or of bleach with ammonia, which produces chloramine gas.
Maintain a patent airway and adequate oxygenation.
Treat bronchospasm with bronchodilators. Severe cough may require narcotic antitussives. Treat noncardiogenic pulmonary edema with oxygen, mechanical ventilation, and PEEP as needed (see Chapter 8, Critical Care).
Treat skin burns by copious irrigation, removal of contaminated clothing, and tetanus prophylaxis (see Appendix F, Immunizations and Postexposure Therapies), if needed. Irrigate the eyes immediately and copiously with water or saline if the patient has had chemical contact.
Obtain ophthalmologic consultation for caustic eye burns.
Risk Management
Because the development of pulmonary edema may be delayed, observe asymptomatic patients with normal ABGs and chest radiographs for at least 6 hours.
Hospitalize patients with symptoms or signs of upper airway edema or pulmonary involvement.
Simple Asphyxiants
These include acetylene, argon, ethane, helium, hydrogen, nitrogen, methane, butane, neon, carbon dioxide, natural gas, and propane, all of which cause hypoxia by displacing oxygen from the inspired air.
Morbidity and mortality are related to the extent and duration of the hypoxia.
Supplemental oxygen
Supportive care for symptomatic patients
Systemic Toxic Inhalants
These are gases that are capable of producing prominent systemic toxicity; they include hydrogen sulfide, methyl bromide, organophosphates, carbon monoxide, and hydrogen cyanide.
Treatment consists of supportive care and specific therapy directed toward the offending agent.
Carbon Monoxide
Poisoning usually occurs in poorly ventilated areas in which carbon monoxide (CO) is released by fires, combustion engines, or faulty stoves or heating systems. Intoxication is seasonal, with more cases occurring in winter.
CO displaces oxygen from hemoglobin, shifts the oxyhemoglobin dissociation curve to the left, and depresses cellular respiration by inhibiting the cytochrome oxidase system.
Direct binding to cardiac myoglobin depresses cardiac function. Toxic manifestations are a consequence of tissue hypoxia.
Symptoms correlate imperfectly with the carboxyhemoglobin level.
Carboxyhemoglobin levels of 20%÷40% are associated with dizziness, headache, weakness, disturbed judgment, nausea and vomiting, and diminished visual acuity. These symptoms and seasonality frequently lead to a misdiagnosis of influenza. Examination may reveal retinal hemorrhages.
Levels of 40%÷60% are associated with tachypnea, tachycardia, ataxia, syncope, and seizures. The ECG may reveal ST-segment changes, conduction blocks, and atrial or ventricular arrhythmias.
Levels >60% are associated with coma and death. Cherry-red coloration of the lips or skin is a relatively rare, late manifestation. Late complications include basal ganglia infarction and parkinsonism. Less severe, delayed neuropsychiatric symptoms also may occur.
Laboratory Studies
Obtain electrolytes, CPK, ABGs, and an ECG, and monitor the cardiac rhythm continuously.
Arterial oxygen tension usually is normal; thus, the diagnosis of carbon monoxide poisoning requires a high level of suspicion and direct measurement of arterial oxygen saturation or carbon monoxide (carboxyhemoglobin) levels. Standard pulse oximetry is not reliable.
Administer 100% oxygen by tight-fitting mask or endotracheal tube. The latter ensures tissue oxygen delivery and decreases the half-life of carboxyhemoglobin from 4÷5 hours to 90 minutes. Measure carboxyhemoglobin levels q2÷4h, and continue oxygen administration until blood levels are <10%.
Hyperbaric oxygen (3 atm) has been strongly recommended for patients who have been unconscious at any time and present with neurologic signs or symptoms, ECG changes consistent with ischemia, severe metabolic acidosis, rhabdomyolysis, pulmonary edema, or shock. Hyperbaric treatment of patients who have minor or no symptoms but who have carboxyhemoglobin levels of >25%÷30% is controversial, as is treatment in pregnancy.
Hyperbaric oxygen appears to improve long-term neurologic outcome.88 Consult with an expert in the field when indications are unclear. In no case should patients be transferred to a hyperbaric oxygen facility until their condition is stabilized. Treat seizures
with diazepam and phenytoin (see Chapter 24, Neurologic Disorders). Arrhythmias and rhabdomyolysis are treated as described elsewhere.
Hydrogen Cyanide
Hydrogen cyanide may be present in industrial fumigants, insecticides, and products of combustion of synthetics and plastics. It may be generated as a byproduct of phencyclidine manufacture.
It has a characteristic bitter almond odor. Toxic amounts are absorbed rapidly through the bronchial mucosa and alveoli, and symptoms usually appear seconds after inhalation. Concentrations of 0.2÷0.3 mg/L air are almost immediately fatal.
Oral exposures to potassium cyanide may be due to rodenticides, insecticides, silver polish, artificial fingernail remover (acetonitrile), film developer, laboratory reagents, and amygdalin.
Symptoms include headache, palpitations, dyspnea, and mental status depression, which may progress quickly to coma, seizures, and death. ECG changes include atrial fibrillation, ventricular ectopy, and abnormal ventricular repolarization.
Severe lactic acidosis is present, and venous oxygen content is higher than normal and may approach arterial oxygen content. Do not delay initiation of therapy for measurement of whole-blood cyanide levels.
Treatment focuses on conversion of hemoglobin to methemoglobin, which binds to the cyanide ion, sparing vital oxidative enzymes.
Amyl nitrite (one broken pearl held under the nostril for 15÷30 sec/min, repeated every minute, with a new pearl q3min) produces a methemoglobin level of approximately 5%. This should be followed as rapidly as possible with 10 mL 3% sodium nitrite IV (0.3 g over 3÷5 minutes). If the response is inadequate, one-half of the dose of sodium nitrite should be repeated in 30 minutes. The goal is a measured methemoglobin level of 30%.
Give sodium thiosulfate (50 mL of a 25% solution IV) immediately after the sodium nitrite, as it converts the cyanide into thiocyanate, which is excreted in the urine. Repeat one-half the dose in 30 minutes if the response is inadequate.
Administer 100% oxygen at all times during treatment to ensure adequate tissue oxygen delivery despite methemoglobinemia.
Do not give methylene blue for methemoglobin levels <70%, as cyanide may be released.
In the event of life-threatening methemoglobinemia, consider exchange transfusion.
Monitor the cardiac rhythm continuously.
For severe persistent acidosis (pH <7.2), administer sodium bicarbonate, 1 mEq/kg, after the preceding measures have been undertaken.
In the event of oral ingestion, empty the stomach by gastric lavage after the preceding measures have been undertaken. Do not induce emesis. Rapid absorption makes administration of activated charcoal of dubious utility.
The efficacy of hyperbaric oxygen is controversial but can be considered for those who respond poorly to conventional therapy.
The FDA recently approved hydroxycobalamin for the treatment of cyanide poisoning (Cyanokit®). Experience in Europe for more than ten years shows that this is a safe and effective alternative to the above regimen. The dose is 5 grams (two vials) in 100 mL normal saline IV over 15 minutes; if the response is inadequate, a second dose of 5 grams may be administered over 15 minutes (for a patient in extremis) to 2 hours (for the less severely affected). Dicobalt ethylenediaminetetra-acetic acid (dicobalt EDTA) and dimethylaminophenol are antidotes that are not available in the United States. If dicobalt EDTA is available, the dose is 300÷600 mg (20÷40 mL) IV over 1÷5 minutes, followed by a 50-mL flush with D5W. An additional 300 mg can be given in 5 minutes if the clinical response is inadequate.
Hydrogen Sulfide
Hydrogen sulfide is a colorless gas with a characteristic rotten-egg odor. It is found in mines and sewers as well as petrochemical, agricultural (liquid manure processing), and tanning industries.
Exposure to low concentrations of hydrogen sulfide causes mucous membrane and eye irritation and vision changes.
Higher concentrations cause cyanosis, confusion, pulmonary edema, coma, and convulsions. Rapid death occurs in approximately 6% of cases.
Therapy is similar to that used for hydrogen cyanide. Oxygen therapy at 100% and nitrites are used, but thiosulfate is not. The efficacy of nitrites is controversial.89
Flush the mucous membranes with saline or water. Consider hyperbaric oxygenation for severe intoxication.
Smoke Inhalation
This is the cause of death in more than 50% of fire-related fatalities. Thermal injury usually is confined to the upper airway because of the rapid cooling of inhaled gases that occurs proximal to the larynx.
Toxic gases released by fire include carbon dioxide, carbon monoxide, hydrogen chloride, phosgene, chlorine, benzene, isocyanate, hydrogen cyanide, aldehydes, oxides of sulfur and nitrogen, ammonia, and numerous organic acids.
Carbon monoxide accounts for 80% of mortality in the first 12 hours. The other toxins produce epithelial injury that results in airway edema, increased capillary permeability, and mechanical obstruction from desquamated tissue and secretions.
Patients who have lost consciousness, have been exposed to a large quantity of smoke in a closed space, have suffered prolonged inhalation or steam exposure, were involved in an explosion, were with other persons who died or were severely injured, or have sustained facial burns or singed nasal vibrissae are at risk for development of respiratory complications, which may be delayed in onset for up to 3 days.
Clinical Presentation
Asphyxiation, expectoration of carbonaceous sputum, hoarseness, dyspnea from upper airway edema, stridor, bronchospasm, and noncardiogenic pulmonary edema are characteristic features of smoke inhalation.
Upper airway burns may also be noted.
Neurologic manifestations include stupor and coma.
Late complications include bacterial pneumonia and pulmonary embolism.
Obtain CBC, electrolytes, ABGs, chest radiograph, ECG, and carboxyhemoglobin level.
High-risk patients should undergo upper airway endoscopy to rule out any life-threatening airway injury immediately; bronchoscopy rarely provides additional therapeutically useful information.
A positive xenon scan predicts increased mortality but is rarely justified.
Carboxyhemoglobin levels that exceed 15% are indicative of severe exposure.
Scrupulous airway care is essential, with frequent suctioning as needed.
Endotracheal intubation is required in patients who display evidence of significant upper airway edema or respiratory insufficiency.
Bronchoscopy may be necessary to remove endotracheal debris. Administer humidified oxygen to all patients.
Give bronchodilators for bronchospasm.
Treat ARDS with mechanical ventilation and PEEP. High-frequency flow interruption ventilation has been reported to be effective90 but is not widely available and requires additional confirmation.
Prophylactic antibiotics and glucocorticoids are not indicated.
Treat specific intoxications (e.g., cyanide and carbon monoxide poisoning) appropriately. Suspect cyanide intoxication if coma and significant lactic acidosis are present.
Patients who have experienced minor smoke inhalation, who are asymptomatic at 4÷6 hours, and who exhibit none of the risk factors just listed can be safely discharged home.
Admit asymptomatic patients who have any risk factors for potential respiratory complications for a minimum of 24 hours.
Admit patients who have symptoms, significant laboratory abnormalities, or an abnormal alveolar-arterial oxygen gradient to an ICU.
1. 2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation 2005;112(Supp 24):IV19÷IV34.
2. Baumann MH, Strange C, Heffner JE, et al. Management of spontaneous pneumo- thorax: an American College of Chest Physicians Delphi consensus statement. Chest 2001;119:590.
3. Noakes TD. Fluid and electrolyte disturbances in heat illness. Int J Sports Med 1998;19:S146.
4. Dematte JE, O'Mara K, Buescher J, et al. Near-fatal heat stroke during the 1995 heat wave in Chicago. Ann Intern Med 1998;129:173.
5. Eichner ER. Treatment of suspected heat illness. Int J Sports Med 1998;19(Supp 2):S150.
6. Gaffin SL, Gardner JW, Flinn SD. Cooling methods for heatstroke victims. Ann Intern Med 2000;132:678.
7. Armstrong LE, Crago AE, Adams R, et al. Whole-body cooling of hyperthermic runners: comparison of two field therapies. Am J Emerg Med 1996;14:355.
8. White JD, Riccobene E, Nucci R, et al. Evaporation versus iced gastric lavage treatment of heatstroke: comparative efficacy in a canine model. Crit Care Med 1987;15:748.
9. Boucham A, Cafege A, Deval EB, et al. Ineffectiveness of dantrolene sodium in the treatment of heatstroke. Crit Care Med 1991;19:176.
10. Briner WW. Tympanic membrane vs. rectal temperature measurement in marathon runners. JAMA 1996;276:194.
11. Hansen RD, Amos D, Leake B. Infrared tympanic temperature as a predictor of rectal temperature in warm and hot conditions. Aviat Space Environ Med 1996;67:1048.
12. Swain JA. Hypothermia and blood pH. A review. Arch Intern Med 1998;148:1643.
13. Delaney KA, Howland MA, Vassalo S, et al. Assessment of acid-base disturbances in hypothermia and their physiologic consequences. Ann Emerg Med 1989;18:72.
14. Golden FS, Hervey GR, Tipton MJ. Circum-rescue collapse: collapse, sometimes fatal, associated with rescue of immersion victims. J Royal Naval Med Serv 1991;77:139.
15. Vanggaard L, Eyolfson D, Xu X, et al. Immersion of distal arms and legs in warm water (AVA rewarming) effectively rewarms mildly hypothermic humans. Aviat Space Environ Med 1999;70:1081.
16. Weinberg AD. The role of inhalation re-warming in the early management of hypothermia. Resuscitation 1998;36:101.
17. Miller JW, Danzl DF, Thomas DM. Urban accidental hypothermia: 135 cases. Ann Emerg Med 1980;9:456.
18. Hall KN, Syverud SN. Closed thoracic cavity lavage in the treatment of severe hypothermia in human beings. Ann Emerg Med 1990;19:204.
19. Walpoth BH, Walpoth-Aslan BN, Mattle HP, et al. Outcome of survivors of accidental deep hypothermia and circulatory arrest treated with extracorporeal blood warming. N Engl J Med 1997;337:1500.
20. Rosen P, Stoto M, Harley I. The use of the Heimlich maneuver in near-drowning: Institute of Medicine report. J Emerg Med 1995;13:397.
21. Gonzales-Rothi R. Near-drowning: consensus and controversies in pulmonary and cerebral resuscitation. Heart Lung 1987;16:474.
22. Bohn DJ, Biggar WD, Smith CR, et al. Influence of hypothermia, barbiturate therapy, and intracranial pressure monitoring on morbidity and mortality after near-drowning. Crit Care Med 1986;14:529.
23. Nussbaum E, Maggi JC. Pentobarbital therapy does not improve neurologic outcome in nearly drowned, flaccid-comatose children. Pediatrics 1988;81:630.
24. Anker AL, Santora T, Spivey W. Artificial surfactant administration in an animal model of near-drowning. Acad Emerg Med 1995;2:204.
25. Perez-Benavides F, Riff E, Franks C. Adult respiratory distress syndrome and artificial surfactant replacement in the pediatric patient. Pediatr Emerg Care 1995;11:153.
26. Pratt FD, Haynes BE. Incidence of “secondary drowning” after saltwater submersion. Ann Emerg Med 1986;15:1048.
27. Watson WA, Litovitz TL, Rodgers GC, et al. 2004 Annual Report of the American Association of Poison Control Centers toxic exposure surveillance system. Am J Emerg Med 2005;23:589.
28. Spivey WH. Flumazenil and seizures: analysis of 43 cases. Clin Ther 1992;14:292.
29. Tenenbein M, Cohen S, Sitar DS. Efficacy of ipecac-induced emesis, orogastric lavage, and activated charcoal for acute drug overdose. Clin Ther 1992;14:292.
30. Kulig K, Bar-Or D, Cantrill SV, et al. Management of acutely poisoned patients without gastric emptying. Ann Emerg Med 1985;14:562.
31. Pond SM, Lewis-Driver DJ, Williams GM, et al. Gastric emptying in acute overdose: a prospective randomized controlled trial. Med J Aust 1995;163:345.
32. Chyka M, Seger D. Position statement: single-dose activated charcoal. J Toxicol Clin Toxicol 1997;35:721.
33. Anonymous. Position statement and practice guidelines on the use of multi-dose activated charcoal in the management of acute poisoning. J Toxicol Clin Toxicol 1999;37:731.
34. Jones AL, Volans G. Management of self-poisoning. BMJ 1999;319:1414.
35. Albertson TE, Derlet RW, Foulke GE, et al. Superiority of activated charcoal alone compared with ipecac and activated charcoal in the treatment of acute toxic ingestions. Ann Emerg Med 1989;18:56.
36. Anonymous. Position paper: ipecac syrup. J Toxicol Clin Toxicol 2004;42:133.
37. Vale JA, Kulig K. Position paper: gastric lavage. J Toxicol Clin Toxicol 2004;42:933.
38. Anonymous. Position paper: cathartics. J Toxicol Clin Toxicol 2004;42:243.
39. Anonymous. Position paper: whole bowel irrigation. J Toxicol Clin Toxicol 2004;42:843.
40. Bond GR, Hite LK. Population-based incidence and outcome of acetaminophen poisoning by type of ingestion. Acad Emerg Med 1999;6:1115÷1120.
41. Acetaminophen. In: Poisindex® System [Internet database]. Greenwood Village, CO: Thomson Micromedex. Updated periodically.
42. Buckley NA, Whyte IM, O'Connell DL, et al. Activated charcoal reduces the need for N-acetylcysteine treatment after acetaminophen (paracetamol) overdose. J Toxicol Clin Toxicol 1999;37:753.
43. Harrison PM, Keays R, Bray GP, et al. Improved outcome of paracetamol-induced fulminant hepatic failure by late administration of acetylcysteine. Lancet 1990;335:1572.
44. Bailey B, McGuigan MA. Management of anaphylactoid reactions to intravenous N-acetylcysteine. Ann Emerg Med 1998;31:710.
45. Bremner JD, Wingard P, Walshe TA. Safety of mirtazapine in overdose. J Clin Psychiat 1998;59:233.
46. Boehnert MT, Lovejoy FH Jr. Value of the QRS duration versus the serum drug level in predicting seizures and ventricular arrhythmias after an acute overdose of tricyclic antidepressants. N Engl J Med 1985;313:474.
47. Wolfe TR, Caravati EM, Rollins DE. Terminal 40-ms frontal plane QRS axis as a marker for tricyclic antidepressant overdose. Ann Emerg Med 1989;18:348.
48. Bosse GM, Barefoot JA, Pfeifer MP, et al. Comparison of three methods of gut decontamination in tricyclic antidepressant overdose. J Emerg Med 1995;13:203.
49. Borys DJ, Setzer SC, Ling LJ, et al. Acute fluoxetine overdose: a report of 234 cases. Am J Emerg Med 1992;10(2):115÷120.
50. Grundemar L, Wohlfart B, Lagerstedt C, et al. Symptoms and signs of severe citalopram overdose. Lancet 1997;349:1602.
51. Barbey JT, Roose SP. SSRI safety in overdose. J Clin Psychiat 1998;59(Suppl 15):42.
52. Alkalis. In: Poisindex® System [Internet database]. Greenwood Village, CO: Thomson Micromedex. Updated periodically.
53. Ethanol. In: Poisindex® System [Internet database]. Greenwood Village, CO: Thomson Micromedex. Updated periodically.
54. Weiss M, Thurnheer U. The osmotic gap in the diagnosis of alcoholic intoxication. Schweiz Medizin Woch J Suisse Med 1988;118:845.
55. Purssell RA, Pudek M, Brubacher J, et al. Derivation and validation of a formula to calculate the contribution of ethanol to the osmolalgap. Ann Emerg Med 2001;38:653.
56. Brent J, McMartin K, Phillips S, et al. Methylpyrazole for Toxic Alcohols Study Group. Fomepizole for the treatment of methanol poisoning. N Engl J Med 2001;344(6):424÷429.
57. Methanol. In: Poisindex® System [Internet database]. Greenwood Village, CO: Thomson Micromedex. Updated periodically.
58. Winter ML, Ellis MD, Snodgrass WR. Urine fluorescence using a Wood's lamp to detect the antifreeze additive sodium fluorescein: a qualitative adjunctive test in suspected ethylene glycol ingestions. Ann Emerg Med 1990;19:633.
59. Wallace KL, Suchard JR, Curry SC, et al. Diagnostic use of physicians' detection of urine fluorescence in a simulated ingestion of sodium fluorescein-containing antifreeze. Ann Emerg Med 2001;38:49.
60. Jacobsen D. New treatment for ethylene glycol poisoning. N Engl J Med 1999;340:879.
61. Brent J, McMartin K, Phillips S, et al. Fomepizole for the treatment of ethylene glycol poisoning. Methylpyrazole for Toxic Alcohols Study Group. N Engl J Med 1999;340:832.
62. Barceloux DG, Krenzelok EP, Olson K, et al. American Academy of Clinical Toxicology Practice Guidelines on the Treatment of Ethylene Glycol Poisoning. Ad Hoc Committee. J Toxicol Clin Toxicol 1999;37:537÷560.
63. Ethylene glycol. In: Poisindex® System [Internet database]. Greenwood Village, CO: Thomson Micromedex. Updated periodically.
64. Tomaszewski C, Musso C, Pearson JR, et al. Lithium absorption prevented by sodiumpolystyrenesulfonate in volunteers. Ann Emerg Med 1992;21:1308.
65. Khan NA, Kruse JA. Methemoglobinemia induced by topical anesthesia: a case report and review. Am J Med Sci 1999;318:415.
66. Ward KE, McCarthy MW. Dapsone-induced methemoglobinemia. Ann Pharmacother 1998;32:549.
67. Maio RF, Gaukel B, Freeman B. Intralingual naloxone injection for narcotic-induced respiratory depression. Ann Emerg Med 1987;16:572.
68. Ashton H, Hassan Z. Best evidence topic report. Intranasal naloxone in suspected opioid overdose. Emerg Med J 2006;23:221.
69. Goldfrank L, Weisman RS, Errick JK, et al. A dosing nomogram for continuous infusion intravenous naloxone. Ann Emerg Med 1986;15:566.
70. Wetli CV, Rao A, Rao VJ. Fatal heroin bodypacking. Am J Forensic Med Pathol 1997;18:312.
71. O'Malley GF, Seifert S, Heard K, et al. Olanzapine overdose mimicking opioid intoxication. Ann Emerg Med 1999;34:279.
72. Gabow PA. How to avoid overlooking salicylate intoxication. J Crit Illness 1986;1:77.
73. Gabow PA, Anderson RJ, Potts DE, et al. Acid-base disturbances in the salicylate-intoxicated adult. Arch Intern Med 1978;138:1481.
74. Vertrees JE, McWilliams BC, Kelly HW. Repeated oral administration of activated charcoal for treating aspirin overdose in young children. Pediatrics 1990;85:594.
75. Dunn C, Held JL, Spitz J, et al. Coma blisters: report and review. Cutis 1990;45:423.
76. Eckstein M, Henderson SO, DelaCruz P, et al. Gammahydroxybutyrate (GHB): report of a mass intoxication and review of the literature. Prehosp Emerg Care 1999;3:357.
77. Anderson IB, Kim SY, Dyer JE, et al. Trends in gamma-hydroxybutyrate (GHB) and related drug intoxication: 1999 to 2003. Ann Emerg Med 2006;47:177.
78. Li J, Stokes SA, Woeckener A. A tale of novel intoxication: a review of the effects of gamma-hydroxybutyric acid with recommendations for management. Ann Emerg Med 1998;31:729.
79. Richards JR, Derlet RW, Duncan DR. Methamphetamine toxicity: treatment with a benzodiazepine versus a butyrophenone. Eur J Emerg Med 1997;4:130.
80. Schwartz RH, Miller NS. MDMA (ecstasy) and the rave: a review. Pediatrics 1997;100:705.
81. Isner JM, Estes NA, Thompson PD, et al. Acute cardiac events temporally related to cocaine abuse. N Engl J Med 1986;315:1438.
82. Ettinger NA, Albin RJ. A review of the respiratory effects of smoking cocaine. Am J Med 1989;87:664.
83. Lange RA, Cigarroa RG, Flores ED, et al. Potentiation of cocaine-induced coronary vasoconstriction by beta-adrenergic blockade. Ann Intern Med 1990;112:897.
84. Sporer KA, Firestone J. Clinical course of crack cocaine body stuffers. Ann Emerg Med 1997;29:596.
85. June R, Aks SE, Keys N, et al. Medical outcome of cocaine bodystuffers. J Emerg Med 2000;18:221.
86. Titley OG, Williams N. Theophylline toxicity causing rhabdomyolysis and acute compartment syndrome. Intens Care Med 1992;18:129.
87. Cooling DS. Theophylline toxicity. J Emerg Med 1993;11:415.
88. Weaver LK, Hopkins RO, Chan KJ, et al. Hyperbaric oxygen for acute carbon monoxide poisoning. N Engl J Med 2002;347:1057.
89. Hall AH, Rumack BH. Hydrogensulfide poisoning: an antidotal role for sodium nitrite? Veterin Hum Toxicol 1997;39:152.
90. Lentz CW, Peterson HD. Smoke inhalation is a multilevel insult to the pulmonary system. Curr Opin Pulm Med 1997;3:321.

Submit "25 Medical Emergencies" to Digg Submit "25 Medical Emergencies" to del.icio.us Submit "25 Medical Emergencies" to StumbleUpon Submit "25 Medical Emergencies" to Google Submit "25 Medical Emergencies" to Facebook Submit "25 Medical Emergencies" to Twitter Submit "25 Medical Emergencies" to MySpace

Tags: None Sửa Tags
Chuyên mục
Washington M.of Medical

Bình luận

# Đăng bình luận qua Facebook