Acute Bronchitis

Acute Bronchitis

Susan Davids, MD, MPH and Ralph M. Schapira, MD in Rakel & Bope: Conn's Current Therapy 2008, 60th ed.

Acute bronchitis is one of the most common diagnoses made by primary care physicians in the United States and accounts for nearly 10 million office visits per year. Acute bronchitis is a transient, self-limited inflammatory process of the upper respiratory tract, specifically the trachea and bronchi. Antibiotics are overprescribed to patients with acute bronchitis; this practice has raised significant concern related to the worldwide rise of antibiotic resistance, which is viewed as one of the world's most pressing public health problems.

Acute bronchitis manifests as an acute respiratory illness of less than 3 weeks' duration, with or without sputum production. Acute bronchitis is a clinical diagnosis and must be distinguished from other respiratory diseases, such as pneumonia, acute exacerbation of chronic bronchitis (episode of worsening of symptoms and expiratory airflow obstruction in patients with chronic obstructive pulmonary disease), and the onset of asthma. Most cases of acute bronchitis occur in the fall and winter. The etiology of acute bronchitis is infectious, and viruses appear to be the cause of most cases. Influenzas A and B are the most common viruses isolated, although a wide variety of infectious agents have been identified, such as adenovirus, coronavirus, parainfluenza virus, respiratory syncytial virus, coxsackievirus, Mycoplasma pneumoniae, Bordetella pertussis, and Chlamydia pneumoniae.

Diagnosis of acute bronchitis is based on findings of a prominent cough that may be accompanied by wheezing and sputum production. Most patients are otherwise healthy and without preexisting respiratory disease. Nonspecific constitutional symptoms may also be part of acute bronchitis. Appropriate management of acute bronchitis is essential because it is one of the most common illnesses that present to physicians in the outpatient setting. Antibiotics are often prescribed unnecessarily for acute bronchitis and other respiratory tract illnesses; these prescriptions may potentially lead to adverse events (i.e., allergic reactions and gastrointestinal side effects) and bacterial resistance. Other medications, such as inhaled bronchodilators and antitussives, are often prescribed for acute bronchitis despite questionable evidence to support their routine use.

Pathophysiology of acute bronchitis involves an acute inflammatory response involving the mucosa of the trachea and bronchi, resulting in injury to the respiratory tract epithelium. Sputum production is increased and bronchoconstriction (potentially resulting in airflow obstruction and wheezing) can occur. Positron emission tomography (PET) of a patient with acute bronchitis confirms that the primary inflammatory changes occur in the trachea and bronchi and not the remainder of the lower respiratory track.

CURRENT DIAGNOSIS

1. Normal healthy adult with cough 2. Predominance of cough 3. Lasts 1 to 3 weeks 4. With or without sputum 5. Can be accompanied by other respiratory and constitutional symptoms 6. Absence of abnormal vital signs and physical exam suggesting pneumonia,particularly Heart rate >100 beats per minute Respiratory rate >24 breaths per minute Temperature >100.4°F (38°C) Lung findings suggest a consolidation process

Diagnosis

Cough, phlegm (which may be purulent as both bacteria and viruses can cause purulent sputum), and wheezing help differentiate acute bronchitis from upper respiratory infections such as pharyngitis and sinusitis. Acute bronchitis must be differentiated from acute bacterial pneumonia. The absence of abnormalities in vital signs (heart rate >100 bpm, respiratory rate >24 breath/min, oral temperature >100.4°F [38°C] and physical examination of the chest) supports the diagnosis of acute bronchitis and makes the need for chest radiography unnecessary in most cases. The treatment and outcome of acute bronchitis and pneumonia are very different; a chest radiograph should always be obtained if there is uncertainty about the diagnosis. Chest radiography will demonstrate no lung infiltrates in a patient with acute bronchitis. In contrast, lung infiltrates are present in pneumonia. Pertussis or whooping cough should be considered in adults with cough in the setting of what appears to be an upper respiratory infection, even in those previously immunized. Typically, the cough of pertussis, unlike acute bronchitis, lasts for longer than 3 weeks. Other respiratory diseases, such as previously undiagnosed asthma, can also mimic acute bronchitis, although several features differentiate asthma from acute bronchitis (see Section 12). Rapid testing to diagnose influenza viruses A and B (the most common causes of acute bronchitis) as a cause of acute bronchitis should be considered given the availability of effective treatment if initiated in the first 48 hours.

Treatment

ANTIBIOTICS, INHALED BRONCHODILATORS, AND ANTITUSSIVES

Existing evidence does not support the routine use of antibiotics for uncomplicated cases of acute bronchitis. Although most cases of acute bronchitis are caused by viral infections, upwards of 60% of patients are prescribed antibiotic therapy, which is contributing to the rise of bacterial resistance to commonly used antibiotics. Meta-analyses examining the effectiveness of antibiotic therapy in patients without underlying lung disease suggest no consistent effect of antibiotics on the severity or duration of acute bronchitis. A recent study evaluated children and patients with colored sputum and found that they also did not benefit from antibiotics. This study also found that compared to other populations, the elderly were less likely to benefit from antibiotics. Smokers with acute bronchitis are even more likely to be prescribed antibiotics.

Their response to antibiotics was either equal to or worse than that of nonsmokers.

CURRENT THERAPY

Antibiotics not routinely recommended If influenza is highly probable and patient is presenting within the first 48 hours, consider treatment with : a. Oseltamivir (Tamiflu) 75 mg PO bid with food for 5 days (influenza A/B) b. Zanamivir (Relenza) 10 mg bid by inhalation for 5 days (influenza A/B) [*] c. Amantadine (Symmetrel) 100 mg bid or 200 mg once daily for 5 days (influenza A) [*] d. Rimantadine (Flumadine) 100 mg bid for 5 days (influenza A) In patients with evidence of bronchial hyperresponsiveness, consider treatment with a. β2-agonists for 1 to 2 weeks b. Antitussives in those with cough for 2 to 3 weeks c. Antipyretics and analgesics as needed d. Smoking cessation Education: cough likely to last 3 weeks or more. ' Due to emergence of antiviral resistance, use of these agents has been discouraged by the CDC.

One possible reason for overuse of antibiotics is the concern by physicians about patient satisfaction. Studies show that patients presenting to the doctor expecting antibiotics were more likely to be prescribed antibiotics; studies also suggest that satisfaction is more related to appropriate patient education than to receiving antibiotics. Patient education should include information regarding the duration of symptoms associated with acute bronchitis. It was found that patients presented on average after 9 days of cough and that the cough persisted for an additional 12 days after the physician visit. This information can impart a realistic expectation of illness duration to the patient.

If influenza is highly suspected and the patient presents within 48 hours of the onset of symptoms, rapid diagnostic testing and treatment should be considered. Both amantadine (Symmetrel) and rimantadine (Flumadine) are effective for influenza A, and neuraminidase inhibitors, inhaled zanamivir (Relenza), and oral oseltamivir (Tamiflu) are effective for influenzas A and B. If these medications are initiated within the first 48 hours of symptoms (and ideally within 30 hours), the duration of illness can be shortened.

The evidence supporting the use of inhaled bronchodilators for the treatment of the symptoms has been variable. Two small trials reported a shorter duration of cough with the use of inhaled ß-agonists; another study reported benefit in those with evidence of bronchial hyperresponsiveness. Current recommendations support the use of ß-agonists only in patients with evidence of bronchial hyperresponsiveness (wheezing or spirometry demonstrating a forced expiration volume in 1 second [FEV₁] <80%>

Antitussive agents have not been shown to improve the acute or early cough but did show some improvements in cough lasting longer than 3 weeks. The current recommendations are to use antitussives, namely dextromethorphan (Benylin) or codeine, in patients with cough of 2 to 3 weeks' duration.

Acute uncomplicated bronchitis is most often a viral illness in which antibiotics are not routinely indicated. Patients presenting with an acute respiratory illness, who are younger than 65 years old without existing pulmonary disease or other significant comorbid illness, should have a thorough physical examination, including vital signs. If the vital signs are normal and physical examination of the chest is clear, pneumonia can most likely be ruled out. In patients who present within 48 hours of onset of symptoms, influenza should be considered as effective therapy is available for acute bronchitis caused by influenzas A or B. Otherwise, the evidence for treatment with antibiotics does not support their routine use. Bronchodilators should be considered in those with evidence of bronchial hyperresponsiveness; cough suppressants should be considered in those with 2 to 3 weeks of cough. Patient education is an integral part of the treatment, and patients should receive information that provides realistic expectations regarding the duration of cough.

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Venomous Snakebite

Venomous Snakebite

Epidemiology

Venomous snakes (Fig. 1) of the world belong to the families Viperidae (subfamily Viperinae: Old World vipers; subfamily Crotalinae: New World and Asian pit vipers), Elapidae (including cobras, kraits, coral snakes, and all Australian venomous snakes), Hydrophiidae (sea snakes), Atractaspididae (burrowing asps), and Colubridae (a large family, of which most species are nonvenomous and only a few are dangerously toxic to humans). Bite rates are highest in temperate and tropical regions where the population subsists by manual agriculture. Estimates indicate >5 million bites annually by venomous snakes worldwide, with >125,000 deaths.

Figure 1. Types of highly venomous snakes. (A).The Viperidae, (B). The Elapidae, (C). Hydrophiidae (D). Atractaspididae

Snake Anatomy/Identification

The typical snake-venom apparatus consists of bilateral venom glands located below and behind the eye and connected by ducts to hollow, anterior maxillary teeth. In viperids (vipers and pit vipers), these teeth are long mobile fangs that retract against the roof of the mouth when the animal is at rest. In elapids and sea snakes, the fangs are smaller and are relatively fixed in an erect position. In ~20% of pit viper bites and higher percentages of other snakebites (e.g., up to 75% for sea snakes), no venom is released ("dry" bites). Significant envenomation probably occurs in ~50% of all venomous snakebites.

Differentiation of venomous from nonvenomous snake species can be difficult. Viperids are characterized by somewhat triangular heads (a feature shared with many harmless snakes); elliptical pupils (also seen in some nonvenomous snakes, such as boas and pythons); enlarged maxillary fangs; and, in pit vipers, paired heat-sensing pits (foveal organs) on each side of the head. The New World rattlesnakes generally have a series of interlocking keratin plates (the rattle) on the tip of the tail; the rattle is used to warn potentially threatening intruders. Color pattern is notoriously misleading in identifying most venomous snakes. Many harmless snakes have color patterns that closely mimic venomous snakes found in the same region.

Venoms and Clinical Manifestations

Snake venoms are complex mixtures of enzymes, low-molecular-weight polypeptides, glycoproteins, and metal ions. Among the deleterious components are hemorrhagins that promote vascular leakage and cause both local and systemic bleeding. Proteolytic enzymes cause local tissue necrosis, affect the coagulation pathway at various steps, and impair organ function. Myocardial depressant factors reduce cardiac output, and neurotoxins act either pre- or postsynaptically to inhibit peripheral nerve impulses. Most snake venoms have multisystem effects in their victims.

Envenomations by most viperids and some elapids with necrotizing venoms typically cause progressive local swelling, pain, ecchymosis (Fig. 2), and (over a period of hours or days) hemorrhagic bullae and serum-filled vesicles. In serious bites, tissue loss can be significant (Fig. 3). Systemic findings can include changes in taste, mouth numbness, muscle fasciculations, tachycardia or bradycardia, hypotension, pulmonary edema, hemorrhage (from essentially any anatomic site), and renal dysfunction. Envenomations by neurotoxic elapids such as kraits (Bungarus spp.), many Australian elapids [e.g., death adders (Atractaspis spp.) and tiger snakes (Notechis spp.)], some cobras (Naja spp.), and some viperids [e.g., the South American rattlesnake (Crotalus durissus) and some Indian Russell's vipers (Daboia russelii)] cause neurologic dysfunction. Early findings may consist of cranial nerve weakness (e.g., manifested by ptosis) and altered mental status. Severe poisoning may result in paralysis, including the muscles of respiration, and lead to death due to respiratory failure and aspiration. After elapid bites, the time of onset of venom intoxication varies from minutes to hours depending on the species involved, the anatomic location of the bite, and the amount of venom injected. Sea snake envenomation usually causes local pain (variable), myalgias, rhabdomyolysis, and neurotoxicity; these manifestations are occasionally delayed for hours.

Figure 2. Northern Pacific rattlesnake (Crotalus oreganus oreganus) envenomations. Top: Moderately severe envenomation. Note edema and early ecchymosis 2 h after a bite to the finger. Bottom: Severe envenomation. Note extensive ecchymosis 5 days after a bite to the ankle.

Figure3. Early stages of severe, full-thickness necrosis 5 days after a Russell's viper (Daboia russelii) bite in southwestern India

Treatment

Field Management

The most important aspect of prehospital care of a victim bitten by a venomous snake is rapid delivery to a medical facility equipped to provide supportive care (airway, breathing, and circulation) and antivenom administration. Most first aid recommendations made in the past are of little benefit, and some can actually worsen outcome. It is reasonable to apply a splint to the bitten extremity in order to lessen bleeding and discomfort and, if possible, to keep the extremity at approximately heart level. In developing regions, indigenous people should be encouraged to seek care quickly at health care facilities equipped with antivenoms as opposed to consulting traditional healers.

Although mechanical suction has been recommended in the field management of venomous snakebite for many years, there is now evidence that this intervention is of no benefit and can actually be deleterious in terms of local tissue damage.

Techniques or devices used for centuries in an effort to limit venom spread remain controversial. Lympho-occlusive bandages or tourniquets may limit spread only at the cost of greater local tissue damage, particularly with necrotic venoms. Because tourniquets lead to higher rates of amputation and loss of function, they absolutely should not be used. Elapid venoms that are primarily neurotoxic and have no significant local tissue effects may be localized by pressure-immobilization, in which the entire limb is immediately wrapped with a bandage (e.g., crepe or elastic) and then splinted. The wrap pressure must reach ~40–70 mmHg to be effective. Furthermore, if more than a few minutes from medical care, the victim must be carried out from the scene of the bite. Otherwise, muscular pumping will promote venom dispersal, even in bites to the upper extremities. In short, pressure-immobilization should be used only in cases where the offending snake is reliably identified and has a primarily neurotoxic venom, the rescuer is skilled in pressure-wrap application, and the victim can be carried to medical care—an uncommon combination of conditions. Besides tourniquets, other forbidden measures include incising or cooling the bite site, giving the victim alcoholic beverages, and applying electric shocks. The best first aid advice, as coined by Dr. Ian Simpson of the World Health Organization's Snakebite Treatment Group, is to "do it 'RIGHT'": reassure the victim, immobilize the extremity, get to the hospital, and inform the physician of telltale symptoms and signs.

Hospital Management

In the hospital, the victim should be closely monitored (vital signs, cardiac rhythm, oxygen saturation, urine output) while a history is quickly obtained and a rapid, thorough physical examination is performed. Victims of neurotoxic envenomation should be watched carefully for evidence of difficulty swallowing or respiratory insufficiency, which should prompt definitive securing of the airway by endotracheal intubation. To provide objective evidence of the progression of envenomation, the level of swelling in a bitten extremity should be marked and limb circumferences measured in several locations every 15 min until swelling has stabilized. Large-bore IV access in unaffected extremities should be established. Early hypotension is due to pooling of blood in the pulmonary and splanchnic vascular beds. Later, hemolysis and loss of intravascular volume into soft tissues may play important roles. Fluid resuscitation with isotonic saline should be initiated for clinical shock. If the blood pressure response to administration of crystalloid (20–40 mL/kg) is inadequate, a trial of 5% albumin (10–20 mL/kg) is prudent. If tissue perfusion fails to respond to volume resuscitation and antivenom infusion (see below), vasopressors (e.g., dopamine) can be added. Invasive hemodynamic monitoring (central venous and/or pulmonary arterial pressures) can be helpful in such cases, although obtaining access is risky if coagulopathy has developed.

Blood should be drawn for typing and cross-matching and for laboratory evaluation as soon as possible. Important studies include a complete blood count (to evaluate degree of hemorrhage or hemolysis and effects on platelet count), studies of renal and hepatic function, coagulation studies (to identify consumptive coagulopathy), and testing of urine for blood or myoglobin. In developing regions, the 20-min whole-blood clotting test (WBCT) can be used to diagnose coagulopathy reliably. A few milliliters of fresh blood are placed in a new, plain glass receptacle (e.g., test tube) and left undisturbed for 20 min. The tube is then tipped once to 45° to determine whether a clot has formed. If not, coagulopathy is diagnosed. In severe envenomations or with significant comorbidity, arterial blood gas studies, electrocardiography, and chest radiography may be helpful. Any arterial puncture in the setting of coagulopathy, however, requires great caution and must be performed at an anatomic site amenable to direct-pressure tamponade. After antivenom therapy (see below), laboratory values should be rechecked every 6 h until clinical stability is achieved.

The key to management of venomous snakebite is the administration of specific antivenom. Circulating venom components bind quickly with heterologous antibodies produced in animals immunized with the venom in question (or a very closely related venom). Antivenoms may be monospecific (for a particular snake species) or polyspecific (covering several medically important species in the region) but rarely offer cross-protection against snake species other than those used in their production unless the species are known to have homologous venoms. In the United States, assistance in finding antivenom can be obtained 24 h a day from regional poison control centers.

Indications for antivenom administration in victims of viperid bites include any evidence of systemic envenomation (systemic symptoms or signs; laboratory abnormalities) and (possibly) significant, progressive local findings (e.g., soft tissue swelling crossing a joint or involving more than half the bitten limb in the absence of a tourniquet). Care must be used in determining the significance of isolated soft-tissue swelling as, in many countries, the saliva of some relatively harmless snakes causes mild edema at the bite site. In such bites, antivenoms are unhelpful and unnecessary.

In the developing world (e.g., much of Asia and Africa), elapid bites are generally treated similarly to viperid bites. Systemic symptoms such as ptosis, other manifestations of cranial nerve impairment, or respiratory compromise constitute grounds for antivenom administration. Decisions about antivenom administration to victims with isolated local signs or symptoms are based on the criteria listed above for viperid bites.

Production of the only antivenom currently available in the United States for coral snake bites has been discontinued, and remaining stocks will be exhausted or will expire shortly. Until a suitable substitute is produced or imported, physicians caring for victims of Micrurus bites may have to rely on sound supportive care, especially airway management and respiratory support.

The package insert for the selected antivenom can be consulted regarding species covered, method of administration, starting dose, and need (if any) for re-dosing. The information in antivenom package inserts, however, is not always accurate and reliable. Whenever possible, it is advisable for treating physicians to seek advice from experts in snakebite management regarding indications for and dosing of antivenom. For viperid bites, antivenom administration should generally be continued as needed until the victim shows definite improvement (e.g., stabilized vital signs, reduced pain, restored coagulation). Neurotoxicity from elapid bites may be harder to reverse with antivenom. Once neurotoxicity is established and endotracheal intubation is required, further doses of antivenom are unlikely to be beneficial. In such cases, the victim must be maintained on mechanical ventilation until recovery occurs, which may take days to weeks.

The newest available antivenom in the United States (CroFab; Fougera, Melville, NY) is an ovine, Fab fragment antivenom that covers systemic venom effects of all North American pit viper species and carries a low risk of allergic sequelae. Table 1 compares the two antivenoms recently available for the treatment of pit viper bites in the United States. The manufacturer of Antivenin (Crotalidae) Polyvalent has recently discontinued its production, leaving CroFab as the current drug of choice for the management of indigenous pit viper envenomations in the United States. Use of any heterologous serum product carries a risk of anaphylactoid reactions and delayed-hypersensitivity reactions (serum sickness). Skin testing for potential allergy is insensitive and nonspecific and should be omitted. Worldwide, the quality and availability of antivenoms are highly variable. In many developing countries, antivenom resources are scarce, contributing to high morbidity and mortality rates in these regions. The rates of acute anaphylactoid reactions to some of these products exceed 50%. If the risk of allergic reaction is significant, pretreatment with appropriate loading doses of IV antihistamines (e.g., diphenhydramine, 1 mg/kg to a maximum of 100 mg; and cimetidine, 5–10 mg/kg to a maximum of 300 mg) may be considered. In some regions, a prophylactic SC or IM dose of epinephrine is given in an effort to reduce the risk of reaction. Further research is necessary to determine whether any pretreatment measures are truly beneficial. Modest expansion of the patient's intravascular volume with crystalloids could blunt an acute adverse reaction.

Table 1 Comparison of Antivenoms Recently Available for Treatment of Pit Viper Bites in the United States

Antivenin (Crotalidae) Polyvalenta CroFabb Available since 1954 2000 Origin Equine Ovine Snakes used in manufacture Crotalus adamanteus C. adamanteus C. atrox C. atrox C. durissus terrificus C. scutulatus Bothrops atrox Agkistrodon piscivorus Snakes covered All North, Central, and South American and some Asian pit vipers All North American pit vipers (and possibly other Latin American pit vipers) Contains IgG, equine albumin Fab fragments Skin testing recommended by manufacturer Yes No Pretreatment with antihistamines recommended Yes No Dosing (for North American pit viper bites only)c Dry bite None None Mild 0 or 5 vials 4 vials Moderate 10 vials 4–6 vials Severe 15–20 vials 6 vials Repeat dosing As needed Repeat starting dose if patient fails to stabilize. After stabilization, give 2 vials q6h for 3 more doses. (Alternatively, re-dose on an as-needed basis with close observation for recurrence of abnormalities.) Volume of diluent 1000 mLd 250 mL Administer over 2 h 1 h Incidence of anaphylactic/-oid reaction 23–56%e 14%f Incidence of delayed serum sickness 18–86%g 3%

aWyeth-Ayerst Laboratories, Philadelphia, PA. bFougera, Melville, NY. cDegrees of envenomation: mild = progressive local findings (no systemic findings and normal laboratory tests); moderate = local findings plus either mild systemic findings or mild laboratory abnormalities; and severe = local findings plus either severe systemic findings or severe laboratory abnormalities. dReduce for children and for patients with congestive heart failure. eSome reactions have been severe, and some have been fatal. fTo date, all reactions have been relatively mild. gIncidence is higher with larger doses.

Pretreatment is not recommended by the manufacturer of CroFab. Epinephrine should, however, always be immediately available, and the antivenom dose to be administered should be diluted in an appropriate volume of crystalloid according to the package insert. Antivenom should be given only by the IV route, and the infusion should be started slowly, with the physician at the bedside during the initial period to intervene immediately at the first signs of any acute reaction. The rate of infusion can be increased gradually in the absence of a reaction until the full starting dose has been administered (over a total period of ~1 h). Further antivenom may be necessary if the patient's clinical condition fails to stabilize or worsens. After stabilization, additional doses of CroFab are often recommended as the small-molecular-weight Fab fragments are rapidly cleared from the circulation. Larger, whole IgG or F(ab)2 antivenoms have longer half-lives that eliminate the need for re-dosing after initial stabilization unless definitive symptoms of envenomation reappear.

If the patient develops an acute reaction to antivenom, the infusion should be temporarily stopped and the reaction immediately treated with IM epinephrine and IV antihistamine and steroids (Chap. 311). If the severity of envenomation warrants additional antivenom, the dose should be further diluted in isotonic saline and restarted as soon as possible. Rarely, in recalcitrant cases, a concomitant IV infusion of epinephrine may be required to hold allergic sequelae at bay while further antivenom is administered. The patient must be very closely monitored, preferably in an intensive care setting, during such therapy.

Blood products are rarely necessary in the management of the envenomated patient. The venoms of many snake species can cause a drop in platelet count or hematocrit and depletion of coagulation factors. Nevertheless, these components usually rebound within hours after administration of adequate antivenom. If the need for blood products is thought to be great (e.g., for a dangerously low platelet count in a hemorrhaging patient), these products still should be given only after adequate antivenom administration to avoid adding fuel to ongoing consumptive coagulopathy.

Rhabdomyolysis and hemolysis should be managed in standard fashion. Victims who develop acute renal failure should be evaluated by a nephrologist and referred for dialysis (peritoneal or hemodialysis) as needed. Such renal failure, usually due to acute tubular necrosis, is frequently reversible. If bilateral cortical necrosis occurs, however, the prognosis for renal recovery is more grim, and long-term dialysis with possible renal transplantation may be necessary.

Acetylcholinesterase inhibitors (e.g., edrophonium and neostigmine) may promote neurologic improvement in patients bitten by snakes with postsynaptic neurotoxins. Victims with objective evidence of neurologic dysfunction after snakebite should receive a trial of acetylcholinesterase inhibitors as outlined in Table 2. If they respond, additional doses of long-acting neostigmine can be continued as needed. Special vigilance is required to prevent aspiration if repetitive dosing of neostigmine is used in an attempt to obviate endotracheal intubation.

Table 2 Use of Acetylcholinesterase Inhibitors in Neurotoxic Snake Envenomation

1. Patients with clear, objective evidence of neurotoxicity after snakebite (e.g., ptosis or inability to maintain upward gaze) should receive a trial of edrophonium (if available) or neostigmine. a. Pretreat with atropine: 0.6 mg IV (children, 0.02 mg/kg; minimum of 0.1 mg) b. Follow with: Edrophonium: 10 mg IV (children, 0.25 mg/kg) or Neostigmine: 1.5–2.0 mg IM (children, 0.025–0.08 mg/kg) 2. If objective improvement is evident at 5 min, continue neostigmine at a dose of 0.5 mg (children, 0.01 mg/kg) every 30 min as needed, with continued administration of atropine by continuous infusion of 0.6 mg over 8 h (children, 0.02 mg/kg over 8 h). 3. Maintain vigilance regarding aspiration risk, and secure the airway with endotracheal intubation as needed.

Care of the bite wound includes application of a dry sterile dressing and splinting of the extremity with padding between the digits. Once the administration of an indicated antivenom has been initiated, the extremity should be elevated above heart level to relieve edema. Tetanus immunization should be updated as appropriate. Prophylactic antibiotics are generally unnecessary after bites by North American snakes, as the incidence of secondary infection is low. Antibiotics can be considered, however, if misguided first-aid efforts have included incisions or mouth suction. In some regions of the world, secondary bacterial infection is more common and the consequences are dire. In these regions, prophylactic antibiotics (e.g., cephalosporins) are commonly used.

Most snake envenomations involve subcutaneous deposition of venom. On occasion, however, venom can be injected more deeply into muscle compartments. If swelling in the bitten extremity raises concern that subfascial muscle edema may be impeding tissue perfusion (muscle-compartment syndrome), intracompartmental pressures (ICPs) should be checked by any minimally invasive technique—e.g., wick catheter or ICP monitor (Stryker Instruments, Kalamazoo, MI). If any ICP is high (>30–40 mmHg), the extremity should be kept elevated while further antivenom is given. A dose of IV mannitol (1 g/kg) can be given in an effort to reduce muscle edema if the patient's hemodynamic status is stable. If, after 1 h of such therapy, the ICP remains elevated, a surgical consultation for possible fasciotomy should be obtained. While evidence from studies of animals suggests that fasciotomy may actually worsen myonecrosis, compartmental decompression is still required to preserve nerve function. Fortunately, the incidence of muscle-compartment syndrome is very low following snakebite.

Wound care in the days after the bite may require careful aseptic debridement of clearly necrotic tissue once coagulation has been restored. Intact serum-filled vesicles or hemorrhagic blebs should be left undisturbed. If ruptured, they should be debrided with sterile technique.

Physical therapy should be started when pain allows in order to return the victim to a functional state. The incidence of long-term loss of function (e.g., reduced range of motion, impaired sensory function) is unclear but is probably quite high (>30%), particularly after viperid bites.

Any patient with signs of venom poisoning should be observed in the hospital for at least 24 h. In North America, a patient with an apparently "dry" viperid bite should be watched for at least 8 h before discharge, as significant toxicity occasionally develops after a delay of several hours. The onset of systemic symptoms is commonly delayed for a number of hours after bites by several of the elapids (including coral snakes), some non–North American viperids [e.g., the hump-nosed pit viper (Hypnale hypnale)], and sea snakes. Patients bitten by these reptiles should be observed in the hospital for at least 24 h. Unstable patients should be admitted to a monitored setting.

At discharge, victims of venomous snakebite should be warned about signs and symptoms of wound infection and serum sickness as well as other potential long-term sequelae, such as pituitary insufficiency in Russell's viper (D. russelii) bites. If the victim had evidence of coagulopathy early on, this abnormality can recur during the first 2–3 weeks after the bite. Such victims should be warned to avoid elective surgery or activities posing a high risk of trauma during this period. Outpatient analgesic treatment and physical therapy should be continued.

In the event of serum sickness (fever, chills, urticaria, myalgias, arthralgias, and possibly renal or neurologic dysfunction developing 1–2 weeks after antivenom administration), the victim should be treated with systemic glucocorticoids (e.g., oral prednisone, 1–2 mg/kg daily) until all findings resolve, at which point the dose is tapered over 1–2 weeks. Oral antihistamines (e.g., diphenhydramine in standard doses) provide additional relief of symptoms.

Morbidity and Mortality

The overall mortality rates for venomous snakebite are low in areas with rapid access to medical care and appropriate antivenoms. In the United States, for example, the mortality rate is <1% for victims who receive antivenom. Eastern and western diamondback rattlesnakes (Crotalus adamanteus and C. atrox, respectively) are responsible for the few snakebite deaths occurring in the United States. Snakes responsible for large numbers of deaths in other regions include cobras (Naja spp.), carpet and saw-scaled vipers (Echis spp.), Russell's vipers (D. russelii), large African vipers (Bitis spp.), lancehead pit vipers (Bothrops spp.), and tropical rattlesnakes (C. durissus).

The incidence of morbidity—defined as permanent functional loss in a bitten extremity—is difficult to estimate but is substantial. Morbidity may be due to muscle, nerve, or vascular injury or to scar contracture. In the United States, such loss tends to be more common and severe after rattlesnake bites than after bites by copperheads (Agkistrodon contortrix) or water moccasins (A. piscivorus).

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Dizziness and Vertigo

Dizziness and Vertigo

Avery Hayes - Kochar's Clinical Medicine for Students, 5th Edition. 2008

Dizziness is one of the most common complaints in clinical practice and affects approximately 20% to 30% of the general population. This symptom is responsible for numerous visits to emergency departments and outpatient clinics. Ongoing dizziness can lead to a loss of function, falls, and injuries. Balance-related falls account for more than one half of all accidental deaths in the elderly. Dizziness is a nonspecific symptom and may be used by the patient to describe a number of different experiences. Because the differential diagnosis is broad, the evaluation of the dizzy patient can be both overwhelming and time consuming.

Differential Diagnosis

Dizziness may be classified into four broad categories based on clinical characteristics, which will provide for more accurate diagnosis (Table 1):

· Vertigo (Table 2) is the illusory sensation of spinning or motion. The patient may feel as if their body or the environment is in motion. Vertigo may be peripheral in etiology, due to disorders of the vestibular end organs (semicircular canals and utricle), eighth cranial nerve, or the vestibular nuclei. Central causes of vertigo include ischemia or damage to brainstem structures, or the cerebellum.

· Presyncope is the sense of impending loss of consciousness due to impaired cerebral blood flow, or anoxia, which often implies an underlying cardiovascular, metabolic, or hematologic disorder.

· Disequilibrium is a sense that one is about to fall, often associated with motor or sensory dysfunction resulting in the inability to maintain balance and gait.

· Lightheadedness describes other nonspecific symptoms related to multiple sensory disturbances, psychiatric illness, and medication side effects that alter the sensorium.

Vertigo

A crucial aspect of the evaluation of vertigo is to differentiate peripheral from central causes (Table 3. The latter have more serious consequences and require emergent evaluation and treatment. The clinical presentation, nature of the nystagmus, and presence of associated neurologic signs and symptoms may help distinguish vertigo of peripheral and central etiologies. Peripheral causes of vertigo often present as abrupt, intense attacks, which last several seconds to minutes, and are accompanied by nausea and vomiting. Vertigo due to central causes may occur with a more gradual onset but have a prolonged duration of symptoms. The intensity of symptoms may be less severe with central causes but often the patient may be unable to stand or walk. Nystagmus associated with peripheral vertigo can be decreased with visual fixation and is typically unidirectional (horizontal with a rotary component). Nystagmus that is purely vertical is due to a central cause. During cases of prolonged vertigo, nystagmus from peripheral causes is diminished by compensation and generally does not last longer than 48 hours.

Table 1 Differential diagnosis of dizziness

Dizziness subtype Type of sensation Temporal characteristics Differential diagnosis Vertigo Spinning or motion Episodic or continuous Benign paroxysmal positional vertigo Meniere’s disease Labyrinthitis Vertebrobasilar ischemia Cerebellar infarction or hemorrhage Presyncope Faint feeling, as though one were about to pass out Episodic, may last seconds, may be relieved by recumbent position Dehydration Ischemic heart disease Obstructive cardiac lesions Cardiac arrhythmia Neurocardiogenic syncope Anemia Hypoglycemia or hyperglycemia Infection Disequilibrium A sense of unsteadiness of the lower extremities Constant but may fluctuate in intensity Multiple sensory deficits including peripheral neuropathy and vision loss Lightheadedness Nonspecific Psychiatric conditions including anxiety, depression, panic attacks, and agoraphobia Hyperventilation Medications

Table 2 Differential diagnosis of vertigo

Peripheral vertigo Central vertigo Benign paroxysmal positional vertigo Cerebellar hemorrhage or infarct Acute vestibular neuritis Labyrinthitis Acoustic neuroma Meniere’sdisease Brainstem ischemia Vertebrobasilar insufficiency

Table 3 Characteristics of peripheral and central vertigo

Characteristics Peripheral Central Severity Severe Mild Onset Sudden Gradual Duration Seconds to minutes Weeks Positional Yes No Fatigable Yes No Associated symptoms Auditory Neurological and visual Nystagmus Horizontal Vertical From Chawala N, Olshaker JS. Diagnosis and management of dizziness and vertigo. Med Clin North Am 2006;90:291-304, with permission.

Because brainstem structures subserve many neurologic functions, infarcts causing vertigo will also have neighborhood effects due to injury to other cranial nerve nuclei, long motor, or sensory tracts. Common presentations are summarized in Table 4. Lateral medullary infarcts cause vertigo by infarction of the vestibular nuclei. Associated symptoms and signs include Horner's syndrome, ipsilateral facial numbness, diplopia, dysphagia, or contralateral limb numbness. Patients with cerebellar infarcts have signs such as dysmetria, past-pointing, or dysdiadochokinesis. Vertigo associated with transient ischemic attack due to vertebrobasilar artery (VBA) insufficiency is associated with additional symptoms such as diplopia, transient blindness, drop attacks, or dysarthria. Stroke in the VBA distribution may have a wide range of findings depending on the branch affected and collateral blood supply. Symptoms include hearing loss, ophthalmoplegia, blindness, sensory loss, and ataxia. Other processes affecting the cerebellum such as hemorrhage may present with headache, severe gait ataxia, or depressed levels of consciousness. The cerebellum may also be involved in demyelinating disorders such as multiple sclerosis.

Peripheral causes of vertigo are more common than central etiologies. Benign paroxysmal positional vertigo (BPPV) is the most common cause of peripheral vertigo. This condition occurs when debris form the utricle forms a plug and circulates within the endolymph of the semicircular canals. This clot is thought to act as a plunger and induce a push-and-pull force on the cupula, creating asymmetric impulses between both ears that result in vertigo and nystagmus. Most patients describe episodes of vertigo that are triggered by changes in head position, such as looking up or rolling over in bed. Attacks are usually sudden in onset and generally last less than 60 seconds. BPPV is characterized by fatigability. The patient will develop tolerance to repeated head movements, causing a reduction in continued symptoms.

Table 4 Stroke syndromes associated with vertigo

Site (artery) Clinical presentation Labyrinth (internal auditory artery) Lateral medullary infarct (vertebral artery, posterior inferior cerebellar artery) Lateral pontomedullary infarction (anterior inferior cerebellar artery) Cerebellum (posterior and anterior inferior cerebellar arteries, superior cerebellar artery) Tinnitus, hearing loss Horner's syndrome, cranial nerves V and VII, crossed sensory loss Horner's syndrome, cranial nerves V and VII, crossed sensory loss, hearing loss Limb dysmetria, ataxia From Delaney K. Bedside diagnosis of vertigo: value of the history and neurologic examination. Acad Emerg Med 2003;10:1388-1395, with permission.

Labyrinthitis and vestibular neuritis are characterized by inflammation; either the canals of the inner ear, vestibular nerve, or nuclei can be affected. Both syndromes can follow a viral upper respiratory infection. Patients usually present with severe vertigo, nausea, and vomiting. Symptoms usually last from days to weeks. The vertigo gradually subsides as the inflammation resolves and central compensatory mechanisms evolve. Otitis media may cause a suppurative labyrinthitis due to bacterial spread form the middle ear through a ruptured membrane or perilymph fistula. These patients appear acutely ill and present with hearing loss and fever in addition to nausea, vomiting, and vertigo. Ramsay-Hunt syndrome is caused by Varicella zoster and is a variant of vestibular neuritis with involvement of the cranial nerves VII and VIII, causing facial paresis, tinnitus, hearing loss, and vertigo.

Meniere’s disease is due to an increase in the volume of endolymph, causing distention of the endolymphatic system. The classic triad is vertigo, tinnitus, and fluctuating sensorineuronal hearing loss. Attacks of vertigo are abrupt and may last from minutes to hours. Attacks also vary in intensity and may be associated with aural fullness or pain. Symptoms can be unilateral or bilateral.

Acoustic neuroma is a benign tumor composed of Schwann cells of the vestibular nerve. Patients often present with tinnitus and hearing loss. These tumors are slow growing and central compensation leads to less severe vertigo. Enlargement of the tumor within the cerebellopontine angle causes compression of the adjacent cranial nerves and brainstem, and may result in facial anesthesia and weakness.

Presyncope

As noted above, presyncope is the sensation that one is about to lose consciousness. Often, this is a milder manifestation of an event that ultimately could result in true syncope. The differential diagnosis and evaluation are the same as for syncope.

Disequilibrium

Dysequilibrium syndrome should be suspected when a patient feels unsteady, as though they are about to fall. This sensation is particularly prominent following a sudden change in position or with loss of visual cues, as when getting on or off an elevator. This phenomenon is triggered by loss of sensory inputs that cue the brain to position or the loss of musculoskeletal function interfering with the minor readjustments in position to maintain balance.

Disequilibrium can be seen in association with a number of disorders including peripheral neuropathy, visual impairment, severe arthritis, and Parkinson's disease. It is particularly common in patients with long-standing diabetes who may have several of these issues present simultaneously.

Lightheadedness

A substantial number of patients with dizziness describe relatively vague symptoms that are difficult to verbalize. Oftentimes these are characterized as a sensation of being lightheaded or floating. A majority of these patients have an underlying psychological issue including anxiety, depression, or increased stress. Physical examination is usually unremarkable. In some of these patients, subclinical hyperventilation may play a role.

Evaluation

Some patients may not be able to give an accurate history; therefore, the physical examination not only serves to differentiate peripheral from central causes of vertigo, but also helps to evaluate for causes of dizziness other than vertigo. Vital signs should be measured, including orthostatic blood pressure.

Physical examination should include a complete eye, ear, nose, and throat examination (looking for nystagmus, asymmetry, or defects in the pupillary reactivity and extraocular movements) and a funduscopic examination to check for papilledema. Inspection of the tympanic membranes should be performed to evaluate for scarring, fluid, or infection. If hearing loss is detected, the Weber and Rinne tuning fork examinations can differentiate between conductive and sensorineural hearing loss. Auscultation for carotid bruits and cardiac examination should be performed to evaluate for potential sources of emboli or obstructive cardiac lesions. A thorough neurological examination is important, including examination of motor strength and sensation, cranial nerves, cerebellar function, Rhomberg's test, and gait.

The Dix-Hallpike maneuver is used to diagnose BPPV (Fig. 1). The patient is seated upright on the examining table with the head held in the hands of the examiner for support. The patient's head is turned 45 degrees toward the side being tested. The patient is rapidly lowered to a supine position with the head hanging below the level of the examining table. The patient should be reminded to keep the eyes open because it is critical to see if vertigo occurs. After a short period of latency, a positive test is indicated by a burst of torsional-vertical nystagmus (the upper poles of the eyes beat torsionally toward the ground) associated with vertigo. The vertigo typically lasts between 20 to 40 seconds and is pathognomonic of the posterior canal variant of BPPV.

Figure 1 Dix-Hallpike maneuver. The patient is positioned with the head hanging 30 to 45 degrees over the table edge first in the midline, which is repeated with the head rotation to right and left. Frames one through four show the procedure in sequence.

If disequilibrium is suspected, it can be helpful to perform a finger touch test. The physician attempts to reproduce the symptom by having the patient turn or change position quickly. In the presence of the symptom, the patient is asked to touch the examiner's finger with their own. If the symptoms improve dramatically, it is very suggestive of disequilibrium.

If the complaint is lightheadedness, the patient should be asked to deliberately hyperventilate. If the symptoms are reproduced, this can help confirm the diagnosis and be used as a tool to reassure the patient.

Laboratory tests may not be helpful if the dizziness is caused by vertigo, but may indicate another cause. Complete blood counts, basic metabolic panel, and thyroid function tests may indicate the presence of anemia, electrolyte abnormalities, hypoglycemia, dehydration, or thyrotoxicosis causing symptoms. Electrocardiography may show signs of atrial fibrillation or ischemia.

Electronystagmography is an examination that records eye movements in response to vestibular, visual, cervical, caloric, rotational, and positional stimulation, and may be used to assess vestibular function. Audiologic evaluation can be performed if indicated to evaluate for patterns of hearing loss.

Patients with suspected central cause of vertigo require cranial imaging with either computed tomography (CT) or magnetic resonance imaging (MRI). CT will identify cerebellar hemorrhage or infarction and suggest the presence of tumor, but lacks the sensitivity to detect small infarcts in the brainstem. MRI has superior sensitivity and will identify small lesions including infarcts, tumors, and plaques. Magnetic resonance angiography will visualize the intracranial vasculature, including the vertebrobasilar system. Patients suspected of having an infarct should also be evaluated for a source of thromboembolism, including electrocardiogram to rule out atrial fibrillation and echocardiogram with a bubble study to evaluate for intracardiac shunt.

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