14 SYSTEMIC EMERGENCIES
Systemic Emergencies in an Office-Based Practice
Nicky R. Holdeman
Most of the problems encountered by an eye care provider are not life threatening, but many conditions can become serious if not identified early and managed appropriately. Eye care providers need to be aware that over the course of one’s career, offices or ASCs are going to be the scene of at least a few emergencies. Therefore, every health care practitioner should be prepared to properly oversee various office emergencies until professional help arrives (i.e., manage iatrogenic complications, initiate resuscitative efforts, stabilize the patient, and make prompt referrals). In addition, one should be able to assess, in most cases, whether a person is experiencing a true emergency, thus summoning EMS appropriately.
The more one can do to reduce the potential for accidents and emergencies, the less chance a patient will be injured, and the less chance the practitioner will be subject to litigation. Dealing successfully with a patient emergency requires preparation, training, and teamwork. Emergency preparedness will vary depending on the type of practice, the transport time to an emergency facility, the types of medications used, and the types of procedures performed. However, there are basic steps each office should take to prepare for emergencies. These steps include the following:
1. Posting current, emergency numbers in various locations throughout the office
2. Keeping a first aid kit and other medical supplies readily available
3. Learning and practicing first aid and CPR—basic life support with automated external defibrillator (AED) training or advanced cardiac life support (ACLS)
4. Preparing and rehearsing emergency procedures with the office staff
5. Ensuring that the office address numbers are posted and easy to read for emergency personnel
Note: The best way to reduce the risk of an emergency in a private office is to know the patient’s medical background. The doctor should establish a complete baseline history on all new patients and update the record on all return patients. A comprehensive history should incorporate the patient’s current medications (including nonprescription drugs, vitamins, dietary supplements, home remedies, and medications not prescribed to the patient), allergies (medications and/or environmental agents), past and current medical conditions, previous surgeries/hospitalizations, and family history. Patients who are most likely to have complications are the elderly, those with advanced comorbid conditions, those taking multiple medications, and those with a history of previous complications. Most would agree that a general eye care provider serves a patient base that is heavily populated with seniors, diabetics, and individuals with vision impairments. Recognizing and recording any predisposing history may help to avoid problems or help to recognize them early should problems occur.
In an office setting, anyone who interacts with patients should have basic CPR training for infants, children, and adults. Doctors should consider being certified in ACLS and should certainly be trained in the use of a defibrillator and in the administration of oxygen and epinephrine.
EQUIPMENT
A standard first aid kit will typically contain an antiseptic ointment, small bandages, scissors, tweezers, Band-Aids, gauze pads, and adhesive tape. In addition, one may consider equipping the office with the following:
- O2 (E-size portable cylinder) with a low flow regulator
- Pocket face mask with one way valve
- Nasal cannula
- Ambu bag or bag-valve mask with an O2 reservoir
- Oropharyngeal airways
- Examination gloves
- Stainless steel basins
- Stethoscope
- Sphygmomanometer with several size cuffs
- Cold/hot packs
- Thermometer
- Glucometer
- 4 × 4 pads
- Skin cleanser (Hibiclens, Betadine)
- Syringes (I.M. 3 cc disposable; S.C. tuberculin)
- Tourniquets
- AED
Given below is a Web site from a large ophthalmic insurer with emergency equipment requirements for coverage: http://www.omic.com/products/bus_products/downloads/OSF%20requirements.rtf
OFFICE EMERGENCY DRUGS
Protocols should be established for common office emergencies, especially those resulting from iatrogenic complications of medications and procedures. Recognition and prompt action lead to appropriate management. Several in-office drugs should be readily available, assuming the proper level of training. These medications include
- Ammonia capsules
- Glucose tablets/paste
- Aspirin
- Bulk saline
- Epinephrine preloaded syringe (AnaKit/ EpiPen)
- Albuterol
- Dexamethasone, hydrocortisone, or methylprednisolone
- Diazepam
- Diphenhydramine
- Glucagon
- Nitroglycerin
- Oxygen
In general, emergencies should be sent immediately, by the best means possible, to a qualified acute care facility. Occasionally, it is unclear whether a patient requires an EMS unit or whether they can be referred to a physician’s office for further management. Some general guidelines to consider would be calling for an ambulance if the victim
- Is unconscious, confused, or seems to be losing consciousness
- Has abnormal vital signs
- Has trouble breathing or is breathing in a strange way
- Has chest pain or pressure
- Has pressure or pain in the abdomen that does not go away
- Has seizures, severe headache, or slurred speech
- Appears to have been poisoned
- Has injuries to the head, neck, or spine
- Has severe bleeding
- Has the possibility of broken bones
- Has paralysis or inability to move
- Has the possibility of broken bones
When summoning Emergency Medical Services (EMS), it is important to follow several basic rules. Each caller should
- Identify themselves
- Supply necessary information to the dispatcher, such as
1. The exact address where the victim is located
2. The telephone number at the scene of the incident
3. What happened to the victim
4. The person(s) involved
5. The condition of the victim
6. The care being given
7. Any special instructions for the drivers
- Hang up last, allowing the dispatcher to hang up first
- Return to offer further assistance
Lastly, it is usually helpful (and courteous) to the EMS and the receiving facility to have a copy of any relevant medical information and examination findings from the referring practitioner. However, copying records should never delay prompt transport of an emergent patient.
For additional information: www.acep.org, American College of Emergency Physicians
Hypoglycemia
Nicky R. Holdeman
ICD-9: 251.2
THE DISEASE
Pathophysiology
Hypoglycemia is a condition in which glucose is moving out of the bloodstream and into cells more rapidly than it is being produced. Since glucose normally furnishes 98% to 100% of the brains’ energy needs, hypoglycemia may result in permanent brain damage or death if emergency care is not provided immediately.
“Clinical hypoglycemia” is described as low blood glucose along with the symptoms and signs consistent with hypoglycemia. While the classic definition of hypoglycemia is a plasma glucose concentration of ≤70 mg/dL, the actual modicum of glucose needed to maintain the brain cells is poorly defined and will vary among different individuals.
Etiology
Hypoglycemia may occur for many reasons (Table 14-1). Most commonly, hypoglycemia results from oral hypoglycemic agents or a relative excess of exogenous insulin in insulin-treated diabetic patients. As intensive (or tight control) therapy increases in order to reduce the well-known complications of diabetes mellitus (DM), the incidence of both mild and severe hypoglycemia (i.e., blood glucose <30 to 35 mg/dL) will also increase.
Less common causes of hypoglycemia include inanition, accidental, and/or malicious acts to induce low glucose levels.
The Patient
Clinical Symptoms
- Headache
- Hunger
- Shakiness
- Visual disturbances (blurred vision, diplopia)
- Tingling and numbness in the extremities
- Dizziness
- Profuse sweating
- Speech difficulties
- Difficulty concentrating, confusion
- Pounding heart (palpitations)
- Hypotension
- Tachycardia
- Full and bounding pulse
- Diaphoresis (cold and clammy)
- Pale skin coloration (pallor)
- Tremors
- Incoordination
- Muscle weakness or paralysis
- Dilated pupils
- Anxiety, nervousness, combativeness, or irritability
- Disorientation, confusion, or changes in personality
- Convulsions, syncope, and/or coma in late stages
Note: In insulin-treated diabetics, it may be difficult to distinguish patients in ketotic hyperglycemia from those with severe hypoglycemia. In contradistinction to severe hyperglycemia, patients with severe hypoglycemia will have no unusual odor on the breath, will manifest normal or depressed respirations, and will appear adequately hydrated. However, if in doubt, administer glucose to the patient in these situations.
Significant History
Since the majority of cases of hypoglycemia result from the effects of exogenous insulin or oral hypoglycemic agents, diabetics should be carefully questioned. The clinician should ask the following:
- Have you eaten today? If so, did you eat less than your doctor recommended?
- Have you taken your insulin today?
- Have you taken your insulin and skipped a meal?
- Have you vomited a meal after taking your insulin?
- Has your diabetes medication(s) or your insulin dosage recently been increased?
- Have you recently worked or exercised strenuously?
- Do you vary the sites of insulin injection?
- Is there a history of infection?
Since drugs other than insulin and conditions besides diabetes may also cause or contribute to clinical hypoglycemia, patients should be questioned regarding the following:
- Renal failure
- Hepatic disease
- Pancreatic tumors (B-cell tumors)
- Excessive ethanol intake
- Aspirin overdose
- Use of β-blockers, pentamidine, or disopyramide
Demographics
The signs and symptoms of hypoglycemia manifest at varying levels among different individuals. Hypoglycemia is much less common among insulin-treated Type 2 diabetic patients than among Type 1 patients. Insulin shock may occur more often in children because of their broadly varied activity and diet.
Ancillary Tests
Determine the patient’s blood glucose by in-office glucometer. The patient should be referred to their primary physician for further evaluation. The physician will differentiate whether the patient has reactive hypoglycemia (e.g., early DM, idiopathic, etc.) or fasting hypoglycemia (e.g., insulinoma, extrapancreatic neoplasms, hepatic or renal failure, insulin reactions, adverse side effects of various medications, ethanol abuse, etc.). Testing to detect or exclude these conditions will be performed as deemed appropriate.
The Treatment
The definitive treatment of hypoglycemia will be determined by identifying the specific underlying disease. However, in-office care may include the following procedures.
If the patient is conscious (mild hypoglycemia), place him or her in a semi-reclining position and give him or her about 15 g of rapidly acting carbohydrates (i.e., commercially repared glucose paste or three glucose tablets). If commercial glucose is not available, 4 oz of juice, a sugar-containing soft drink, corn syrup, honey, jelly, sugar cubes, or hard candy will help to increase the glucose level. It is, however, important not to over treat as there is a risk of inducing a swinging cycle of high and low blood glucose levels.
The goal is to raise the patient’s blood glucose to a minimum level of 70 to 80 mg/dL. It takes about 15 minutes for the carbohydrates to be digested and to enter the blood stream as glucose. After giving the 15 g of rapidly acting carbohydrates, recheck the blood glucose level in 15 minutes (the rule of 15’s). Once the blood glucose level is normalized, provide a small snack containing carbohydrates, fat, and protein to maintain the appropriate blood glucose concentration. Gels or liquids should never be forced into the mouth of an unarousable patient due to the risk of aspiration.
If the patient is unconscious or seizing and cannot swallow (severe hypoglycemia), make sure that there is an adequate airway and administer oxygen if available. If properly trained, the patient should have an indwelling catheter placed in a large vein (e.g., brachial vein) and given 50% dextrose in water, 50 mL at 10 mL/min. Most patients regain consciousness within 5 to 10 minutes.
If an IV is not available or cannot be established, patients more than 10 years of age should be given 1.0 mg of glucagon injected IM or SC in the deltoid or anterior thigh. If the patient is a child, 0.5 mg of glucagon should be administered. Glucagon kits are available by prescription and glucagon can be quickly reconstituted in the office.
Activate EMS and transport immediately to the hospital, even if the patient seems to be completely recovered. Patients with hypoglycemia secondary to oral hypoglycemic agents should be monitored for 24 to 48 hours since hypoglycemia may recur.
Note: A diabetic patient who has a sudden change in mental function or level of consciousness is more likely to be hypoglycemic than hyperglycemic. Consequently, if the patient is a known or suspected diabetic, and insulin shock cannot be excluded, when in doubt, give glucose!
Choking/Airway Obstruction
Nicky R. Holdeman
ICD-9: 934.9
THE DISEASE
Pathophysiology
The organs of the body require a continuous supply of oxygen in order to survive. Thus, an acute obstruction of the airway by foreign material poses a potential life-threatening emergency. Without a patent airway and adequate gas exchange, other resuscitative measures will usually not be successful. Respiration may be interrupted by either obstruction or compression.
Etiology
Choking is a common breathing emergency. Aspiration of any foreign material may cause asphyxia if the substance aspirated is large or the cough reflex is impaired. However, one of the most common obstructions of the upper airway is by food. This condition, often referred to as a “cafe coronary,” could easily occur in an office setting.
The Patient
The clinical presentation of a choking individual will depend on whether the airway is partially or completely blocked and on the site of obstruction. In general, one should look for the following symptoms or signs.
Clinical Symptoms
- Coughing, choking, gagging
- Wheezing
- Difficulty talking
Note: A partially blocked airway can become completely obstructed. A person whose airway is totally blocked cannot speak, cough forcefully, or breathe.
Clinical Signs
- Clutching the throat with one or both hands (the universal distress signal for choking)
- Tachypnea
- Labored breathing with inadequate movement of air
- Stridor
- Substernal notch retraction
- Agitation or lethargy
- Cyanosis
- Rapid pulse initially and then decreased pulse
- Respiratory arrest
- Cardiac arrest
Significant History
History of an aspiration event may be absent in 30% to 50% of patients. Lack of a positive history often delays diagnosis, so foreign bodies should be suspected, especially in children, as the airway is smaller. Aspiration of food is more likely to occur in the following patients:
- Intoxicated individuals
- Those with swallowing difficulties
- Older individuals (≥75)
- Patients with poor dentition
- Denture wearers (difficulty to sense whether food has been fully chewed)
- Those who eat while excited or laughing
- Those who play or run with food in the mouth
- Those who use sedative drugs
- Those who play or run with food in the mouth
Demographics
More than 3,000 deaths annually are due to choking. While most airway obstruction due to foreign bodies occurs between the ages of 1 and 5 years, more adults than children die each year because of choking.
Ancillary Tests
Lab testing per se is not indicated. Ultimately, the patient may have plain radiographic films, fluoroscopy, or bronchoscopy to assist in the diagnosis of airway obstruction. If a foreign body is not recovered, the patient should undergo radiological imaging for localization.
The Treatment
Management of foreign bodies in the airway is dictated by the location of the object and the age and condition of the patient.
If the choking person is coughing, do not interfere; the normal reflexes will often clear the airway. Allow the patient to assume a position that is comfortable and that facilitates respiration.
If there is total obstruction, abdominal thrusts/Heimlich maneuver should be attempted in patients ≥1 year of age. These maneuvers should be repeated until effective or until the patient becomes unresponsive.
In infants (<1 year of age), back blows and chest thrusts are recommended. Continue these maneuvers until the airway has cleared or the patient loses consciousness.
If the foreign body is visible, the airway may be cleared with a manual sweep in an unresponsive patient. Blind sweeps are not recommended.
If there is no success at clearing the airway and if the patient loses consciousness, EMS should be activated. In the meantime, place the patient in a supine position; tilt the head backward and continue to attempt to open the airway; check for respiratory sounds and ventilate if possible. Continue CPR until advanced life support arrives on the scene.
If these methods are unsuccessful, a surgical airway (access to the airway by tracheotomy) may be necessary.
Ultimately, the patient may require removal of the foreign body under general anesthesia with a laryngoscope or bronchoscope.
Syncope
Nicky R. Holdeman
ICD-9: 780.2
THE DISEASE
Pathophysiology
Syncope, or fainting, is a sudden and transient loss of consciousness due to inadequate cerebral blood flow and oxygenation, followed by spontaneous recovery. Except for the risk of physical injury from falling, simple fainting itself is often not a major health concern. However, fainting can be a sign of a serious underlying disorder and must be distinguished from conditions such as epileptic seizures, transient ischemic attacks (TIAs), vertigo, hysteria, and hypoglycemia.
Etiology
An attempt to establish the etiology of syncope is important because the symptom is common and potentially fatal. While the list of possible causes is long and diverse, the major categories include the following:
- Vasovagal (vasomotor) syncope or simple fainting—due to excessive vagal tone resulting in a decrease in both arterial pressure and heart rate. Accounts for 21% of syncopal episodes
- Orthostatic (postural) hypotension—due to a rapid fall in blood pressure, when moving from a supine to upright position. May result from multiple factors such as certain drugs (e.g., antihypertensives), neuropathies (e.g., DM), hypovolemia, or spinal cord injuries. Orthostasis is estimated to cause 9% of syncopal events
- Cardiogenic syncope—involves a wide range of conditions and diseases including dysrythmias, cardiomyopathies, conduction disorders, aortic stenosis, acute myocardial infarctions (AMI), or cardiac tamponade Cardiac conditions account for 10% of syncopal events and have a two- to threefold increase in all-cause mortality. Other causes of syncope include emotional stress, blood loss, heat or dehydration, carotid artery problems, and blood clots in the lung.
- Orthostatic (postural) hypotension—due to a rapid fall in blood pressure, when moving from a supine to upright position. May result from multiple factors such as certain drugs (e.g., antihypertensives), neuropathies (e.g., DM), hypovolemia, or spinal cord injuries. Orthostasis is estimated to cause 9% of syncopal events
The Patient
In general, syncope will be characterized by loss of consciousness, unresponsiveness, loss of postural tone, and spontaneous recovery. However, certain symptoms and signs will often manifest depending on the underlying cause. Since vasovagal episodes are the most common entity seen in outpatient facilities, the following descriptors pertain to this particular type of syncope.
Clinical Symptoms
Clinical symptoms include brief prodrome of warmth, nausea, anxiety, dizziness, light-headedness, weakness, sweating, salivation, and blurred vision. The prodrome usually lasts from 10 seconds to a few minutes.
Clinical Signs
Initially, tachycardia, diaphoresis, and pallor are seen. These signs are soon followed by bradycardia, decreased blood pressure, pupillary dilation, weak pulse, and transient loss of consciousness. Abnormal movements, which may mimic a seizure, are often noted, but urinary incontinence and tongue biting are rare.
Demographics
Vasovagal disorders are very common and occur in all age groups, affecting men and women equally.
Syncope, from all causes, accounts for about 1% to 6% of hospital admissions and about 3% of emergency room visits. Five to twenty percent of adults will have one or more episodes of syncope by age 75.
Significant History
The evaluation for syncope depends heavily on a careful history if the underlying cause is to be discovered. Witnesses to the event may provide additional insight. The clinician should obtain the following information:
- The events leading up to the syncopal episode (e.g., coughing, urinating, defecating)
- Syncope with exertion suggests a cardiac cause
- The patients posture before syncope (e.g., vasovagal syncope does not occur when the patient is horizontal, but cardiac syncope can occur in any position)
- Prodromal manifestations (e.g., syncope with marked sweating and tachycardia is likely the result of hypoglycemia, whereas syncope with mild sweating, nausea, and bradycardia is more often due to a vasovagal episode, especially in circumstances provoking strong emotion. Syncope of sudden onset with brief or no premonitory symptoms suggests a cardiac cause)
- Were there focal neurologic signs? (e.g., neurologic abnormalities such as a motor or sensory loss may suggest transient cerebral ischemia (TIA) and prompts a search for emboli or thrombosis)
- Is there a family history of syncope? (e.g., a family history of syncope suggests migrane, epilepsy, or vasovagal attacks)
- Does the patient have any underlying diseases or comorbid conditions?
- Are they taking any medications? (e.g., several classes of drugs have a predisposition to syncope—doxazosin, terazosin)
- Have they recently ingested drugs or alcohol?
- Is there a family history of syncope? (e.g., a family history of syncope suggests migrane, epilepsy, or vasovagal attacks)
Ancillary Tests
In addition to a careful history, a thorough physical examination and an ECG are important procedures in determining a diagnosis. Depending on the outcome of these standard procedures, a given patient may also require hematology testing and blood chemistries (e.g., CBC, electrolytes, glucose, toxicology), cardiac studies (e.g., transtelephonic ECG, echocardiogram, stress testing, electrophysiologic studies), neurologic investigations (e.g., EEG, CT, or MRI of the head), and/or psychiatric evaluation (e.g., exclude anxiety, depression, alcohol, and drug abuse).
Unfortunately, even after careful evaluation and testing, the cause of syncope will be determined in only 63% of patients.
The Treatment
Since syncopy itself is not a disease but can indicate a wide range of conditions and disorders, the ultimate treatment will be directed toward the underlying etiology. If no serious cause is found, the only interventions that may be necessary are avoiding situations that lead to fainting and protecting from an injury due to a fall.
In-office care should include the following:
- If the person has not yet fainted but becomes pale, begins to perspire, and feels faint, have the patient sit and lower their head to a level between the knees or carefully help place them in a recumbent position.
- If the patient has already fainted, lower the victim to the ground, position them on their back, and elevate the legs 8 to 12 in. (Get their toes above their nose.)
- Loosen any tight clothing, such as a tie or collar that may restrict free breathing or impinge on the carotid sinus.
- Check to make sure the patient is breathing. Establish and maintain an open airway and administer O2, 2 to 3 L/min, by nasal canula if the patient is conscious.
- Place crushed ammonia capsule under the nose.
- Monitor for vomiting and possible aspiration. If the patient vomits, place the victim on his or her side.
- Check vital signs; initiate appropriate emergency care.
- Apply cold compresses to the forehead or to the back of the neck.
- Do not give the victim anything to eat or drink unless hypoglycemia is suspicioned and the victim is fully conscious.
- Check for any injuries that may have been sustained during a fall and treat them appropriately.
- Keep the victim from getting chilled or overheated.
- If the patient manifests abnormal movements or has a seizure, do not hold or restrain the person or place anything between the teeth. Cushion the victim’s head and prevent bodily injury by removing nearby objects. Seizure-like movements are not uncommonly seen in syncopal patients.
- Do not allow a person who has fainted to get up after regaining consciousness. Syncope may recur, especially if the patient stands within 30 minutes after the attack.
- Transport the patient to the emergency room for further management and observation, particularly if the vital signs are unstable and/or if the problem is recurrent.
Note: Vasovagal syncope has an excellent prognosis, and the risk of death is not increased by these events.
For additional information: National Institute of Neurological Disorders and Stoke: www.ninds.nih.gov
Anaphylaxis (Anaphylactic Shock)
Nicky R. Holdeman
ICD-9: 995.0
THE DISEASE
Pathophysiology
Shock is a clinical syndrome defined by an inadequate blood flow and transport of oxygen to organs and tissues. When the body’s organs do not receive blood, they fail to function properly and the potential for irreversible tissue damage occurs.
Anaphylaxis, a form of shock, is a serious condition that is rapid in onset and may cause death. Anaphylaxis is an IgE-mediated, Type 1 allergic reaction to a foreign antigen. This reaction results in massive activation of mast cells, with release of their inflammatory mediators in the skin, respiratory tract, and circulatory system resulting in urticaria, wheezing, and hypotension.
It is thought that the initial exposure to an antigen may result in specific IgE antibodies to that antigen. On re-exposure, the antigen can bind the IgE antibodies on the surface of mast cells and basophils. This cross-linking can result in degranulation and release of vasoactive substances and chemotactic factors such as histamine, tryptase, and other mediators of inflammation into the systemic circulation. These mediators result in vasodilatation, increased vascular permeability, stimulation of nociceptor nerve endings, and smooth muscle spasm in the bronchi and gastrointestinal (GI) tract, producing the clinical symptoms of anaphylaxis.
The severity of an individual’s response is dependent on the rate, amount, and site of mediator release, as well as preexisting medical conditions (e.g., asthma, cardiovascular disease).
Anaphylactoid reactions are clinically similar to anaphylaxis, but may occur after the first exposure of certain drugs or contrast agents. These reactions are not IgE mediated but are rather due to direct activation of mast cells and basophils by certain substances. For practical purposes, it does not matter whether the patient is experiencing true anaphylaxis or an anaphylactoid reaction, as the clinical manifestations and the treatment of both reactions are identical.
Etiology
A growing number of agents can cause anaphylaxis including proteins (e.g. antiserum, insulin, ACTH), enzymes (e.g., insect venoms), pollen (e.g., grass, ragweed), food (e.g., egg white, rice, milk, nuts, shellfish, chocolate), diagnostic agents (e.g., NaFl, radiocontrast media), antibiotics (e.g., penicillin, tetracyclines), NSAIDs, latex products, and/or exercise. Although most cases can be traced to specific trigger factors, up to 20% are designated as idiopathic.
The Patient
After exposure to the offending agent, the clinical features of anaphylaxis can begin within seconds or take as long as an hour to develop. However, the spectrum of symptoms may range from mild to fatal within minutes. The most commonly affected organ systems are the skin (up to 80% of patients), GI tract, respiratory tract, and cardiovascular system (see Table 14-1). Isolated urticaria and angioedema are more common forms of anaphylaxis with a better prognosis. Ominous signs and symptoms are those of progressive respiratory and circulatory failure.
Clinical Symptoms
Generally, the shorter the time before symptoms appear after exposure, the more ominous the prognosis. Patients with immediate allergic reactions are at risk for shock and respiratory arrest.
Symptoms vary, and rarely does one patient develop all the symptoms listed:
- Sense of agitation, panic, or of impending doom
- Itching (particularly of the nose and hands)
- Feeling of warmth (flushed face)
- Sneezing/coughing
- Angioedema
- Watery eyes and nose
- Skin rash
- Sense of throat closing and hoarseness (laryngeal edema)
- Throbbing in the ears
- Nausea/vomiting/diarrhea
- Crampy abdominal pain
- Uterine and bladder cramping
- Light headedness/faintness
- Shortness of breath or labored breathing (bronchospasm)
- Feeling of substernal pressure or chest pain
- Back pain
Clinical Signs
Anaphylaxis is graded by its clinical presentation (Table 14-2). Manifestations may include the following:
- Erythema and angioedema of the skin (painless, subcutaneous swelling, often involving the periorbital, circumoral, and facial regions. Represents vasodilation and escape of plasma into tissues and results in a decrease of effective plasma volume, which is a major cause of shock).
- Pruritis
- Urticaria (large, irregularly shaped pruritic, erythematous wheals)
- Conjunctival injection, lacrimation
- Rhinorrhea
- Coughing, hoarseness, stridor
- Dyspnea, tachypnea, wheezing
- Cyanosis
- Tachycardia, hypotension, arrhythmias
- Vomiting, diarrhea
- Incontinence
- Cognitive difficulties
- Dizziness, weakness, syncope, seizures