Borchers Andrea Ann (ed.) Handbook of Signs & Symptoms 2015

deviations; hematologic, coagulation, renal, and GI disorders; and certain drugs and treatments.

EMERGENCY INTERVENTIONS

If the patient has severe epistaxis, quickly take his vital signs. Be alert for tachypnea, hypotension, and other signs of hypovolemic shock. Insert a large-gauge I.V. line for rapid fluid and blood replacement, and attempt to control bleeding by pinching the nares closed. (However, if you suspect a nasal fracture, don’t pinch the nares. Instead, place gauze under the patient’s nose to absorb the blood.)

Have a hypovolemic patient lie down and turn his head to the side to prevent blood from draining down the back of his throat, which could cause aspiration or vomiting of swallowed blood. If the patient isn’t hypovolemic, have him sit upright and tilt his head forward. Constantly check airway patency. If the patient’s condition is unstable, begin cardiac monitoring and give supplemental oxygen by mask.

History and Physical Examination

If the patient isn’t in distress, take a history. Does he have a history of recent trauma? How often has he had nosebleeds in the past? Have the nosebleeds been long or unusually severe? Has the patient recently had surgery in the sinus area? Ask about a history of hypertension, bleeding or liver disorders, and other recent illnesses. Ask if the patient bruises easily. Find out what drugs he uses, especially anti-inflammatories, such as aspirin, and anticoagulants, such as warfarin. Ask about a history of cocaine use.

Begin the physical examination by inspecting the patient’s skin for other signs of bleeding, such as ecchymoses and petechiae, and noting jaundice, pallor, or other abnormalities. When examining a trauma patient, look for associated injuries, such as eye trauma or facial fractures.

Medical Causes

Aplastic anemia. Aplastic anemia develops insidiously, eventually producing nosebleeds as well as ecchymoses, retinal hemorrhages, menorrhagia, petechiae, bleeding from the mouth, and signs of GI bleeding. Fatigue, dyspnea, a headache, tachycardia, and pallor may also occur.

Barotrauma. Commonly seen in airline passengers and scuba divers, barotrauma may cause severe, painful epistaxis when the patient has an upper respiratory tract infection.

Coagulation disorders. Such coagulation disorders as hemophilia and thrombocytopenic purpura can cause epistaxis along with ecchymoses, petechiae, and bleeding from the gums, mouth, and I.V. puncture sites. Menorrhagia and signs of GI bleeding, such as melena and hematemesis, can also occur.

Glomerulonephritis (chronic). Glomerulonephritis produces nosebleeds as well as hypertension, proteinuria, hematuria, a headache, edema, oliguria, hemoptysis, nausea, vomiting, pruritus, dyspnea, malaise, and fatigue.

Hepatitis. When hepatitis interferes with the clotting mechanism, epistaxis and abnormal bleeding tendencies can result. Associated signs and symptoms typically include jaundice, claycolored stools, pruritus, hepatomegaly, abdominal pain, a fever, fatigue, weakness, dark amber

urine, anorexia, nausea, and vomiting.

Hypertension. Severe hypertension can produce extreme epistaxis, usually in the posterior nose, with pulsation above the middle turbinate. It may be accompanied by dizziness, a throbbing headache, anxiety, peripheral edema, nocturia, nausea, vomiting, drowsiness, and mental impairment.

Leukemia. With acute leukemia, sudden epistaxis is accompanied by a high fever and other types of abnormal bleeding, such as bleeding gums, ecchymoses, petechiae, easy bruising, and prolonged menses. These may follow less noticeable signs and symptoms, such as weakness, lassitude, pallor, chills, recurrent infections, and a low-grade fever. Acute leukemia may also cause dyspnea, fatigue, malaise, tachycardia, palpitations, a systolic ejection murmur, and abdominal or bone pain.

With chronic leukemia, epistaxis is a late sign that may be accompanied by other types of abnormal bleeding, extreme fatigue, weight loss, hepatosplenomegaly, bone tenderness, edema, macular or nodular skin lesions, pallor, weakness, dyspnea, tachycardia, palpitations, and headache.

Maxillofacial injury. With a maxillofacial injury, a pumping arterial bleed usually causes severe epistaxis. Associated signs and symptoms include facial pain, numbness, swelling, asymmetry, open-bite malocclusion or an inability to open the mouth, diplopia, conjunctival hemorrhage, lip edema, and buccal, mucosal, and soft palate ecchymoses.

Nasal fracture. Unilateral or bilateral epistaxis occurs with nasal swelling, periorbital ecchymoses and edema, pain, nasal deformity, and crepitation of the nasal bones.

Nasal tumor. Blood may ooze from the nose when a tumor disrupts the nasal vasculature. Benign tumors usually bleed when touched, but malignant tumors produce spontaneous unilateral epistaxis, along with a foul discharge, cheek swelling, and, in the late stage, pain.

Polycythemia vera. A common sign of polycythemia vera, spontaneous epistaxis may be accompanied by bleeding gums; ecchymoses; ruddy cyanosis of the face, nose, ears, and lips; and congestion of the conjunctiva, retina, and oral mucous membranes. Other signs and symptoms vary according to the affected body system, but may include a headache, dizziness, tinnitus, vision disturbances, hypertension, chest pain, intermittent claudication, early satiety and fullness, marked splenomegaly, epigastric pain, pruritus, and dyspnea.

Sarcoidosis. Oozing epistaxis may occur in sarcoidosis, along with a nonproductive cough, substernal pain, malaise, and weight loss. Related findings include tachycardia, arrhythmias, parotid enlargement, cervical lymphadenopathy, skin lesions, hepatosplenomegaly, and arthritis in the ankles, knees, and wrists.

Scleroma. With scleroma, oozing epistaxis occurs with a watery nasal discharge that becomes foul smelling and crusty. Progressive anosmia and turbinate atrophy may also occur.

Sinusitis (acute). With sinusitis, a bloody or blood-tinged nasal discharge may become purulent and copious after 24 to 48 hours. Associated signs and symptoms include nasal congestion, pain, tenderness, malaise, a headache, a low-grade fever, and red, edematous nasal mucosa.

Skull fracture. Depending on the type of fracture, epistaxis can be direct (when blood flows directly down the nares) or indirect (when blood drains through the eustachian tube and into the nose). Abrasions, contusions, lacerations, or avulsions are common. A severe skull fracture may cause a severe headache, a decreased level of consciousness, hemiparesis, dizziness, seizures, projectile vomiting, and decreased pulse and respiratory rates.

A basilar fracture may also cause bleeding from the pharynx, ears, and conjunctiva as well as

raccoon eyes and Battle’s sign. Cerebrospinal fluid or even brain tissue may leak from the nose or ears. A sphenoid fracture may also cause blindness, whereas a temporal fracture may also cause unilateral deafness or facial paralysis.

Systemic lupus erythematosus (SLE). Usually affecting women younger than age 50, SLE causes oozing epistaxis. More characteristic signs and symptoms include butterfly rash, lymphadenopathy, joint pain and stiffness, anorexia, nausea, vomiting, myalgia, and weight loss. Typhoid fever. Oozing epistaxis and a dry cough are common. Typhoid fever may also cause an abrupt onset of chills and a high fever, vomiting, abdominal distention, constipation or diarrhea, splenomegaly, hepatomegaly, “rose-spot” rash, jaundice, anorexia, weight loss, and profound fatigue.

Other Causes

Chemical irritants. Some chemicals — including phosphorus, sulfuric acid, ammonia, printer’s ink, and chromates — irritate the nasal mucosa, producing epistaxis.

Drugs. Anticoagulants, such as warfarin, and anti-inflammatories, such as aspirin, can cause epistaxis. Cocaine use, especially if frequent, can also cause epistaxis.

Surgery and procedures. Rarely, epistaxis results from facial and nasal surgery, including septoplasty, rhinoplasty, antrostomy, endoscopic sinus procedures, orbital decompression, and dental extraction. Patients who require supplemental oxygen via nasal cannula may be at risk for increased nosebleeds.

Special Considerations

External methods to help control a nosebleed should include having the patient sit upright and lean forward, pinch his nose for 10 minutes, and breathe through his mouth. Until the bleeding is completely under control, continue to monitor the patient for signs of hypovolemic shock, such as tachycardia and clammy skin. If external pressure doesn’t control the bleeding, insert cotton that has been impregnated with a vasoconstrictor and local anesthetic into the patient’s nose.

If bleeding persists, expect to insert anterior or posterior nasal packing. (See Controlling Epistaxis with Nasal Packing, page 293.) Administer humidified oxygen by face mask to a patient with posterior packing.

Controlling Epistaxis with Nasal Packing

When direct pressure and cautery fail to control epistaxis, nasal packing may be required. Anterior packing may be used if the patient has severe bleeding in the anterior nose. Horizontal layers of petroleum jelly gauze strips are inserted into the nostrils near the turbinates.

Posterior packing may be needed if the patient has severe bleeding in the posterior nose or if blood from anterior bleeding starts flowing backward. This type of packing consists of a gauze pack secured by three strong silk sutures. After the nose is anesthetized, sutures are pulled through the nostrils with a soft catheter and the pack is positioned behind the soft palate. Two of the sutures are tied to a gauze roll under the patient’s nose, which keeps the pack in place. The third suture is taped to his cheek. Instead of a gauze pack, an indwelling urinary or nasal

epistaxis catheter may be inserted through the nose into the area behind the soft palate and inflated with 10 mL of water to compress the bleeding point.

PRECAUTIONS

If the patient has nasal packing, follow these guidelines:

Watch for signs of respiratory distress, such as dyspnea, which may occur if the packing slips and obstructs the airway.

Keep emergency equipment (flashlights, scissors, and a hemostat) at the patient’s bedside. Expect to cut the cheek suture (or deflate the catheter) and remove the pack at the first sign of airway obstruction.

Avoid tension on the cheek suture, which could cause the posterior pack to slip out of place.

Keep the call bell within easy reach.

Monitor the patient’s vital signs frequently. Watch for signs of hypoxia, such as tachycardia and restlessness.

Elevate the head of the patient’s bed, and remind him to breathe through his mouth. Administer humidified oxygen as needed.

Instruct the patient not to blow his nose for 48 hours after the packing is removed.

A complete blood count may be ordered to evaluate blood loss and detect anemia. Clotting studies, such as prothrombin time and partial thromboplastin time, may be required to test coagulation time. Prepare the patient for multiple radiology tests if he has had a recent trauma.

Patient Counseling

Teach the patient or caregiver pinching pressure techniques. Discuss ways to prevent nosebleeds.

Pediatric Pointers

Children are more likely to experience anterior nosebleeds, usually the result of nose picking or allergic rhinitis. Biliary atresia, cystic fibrosis, hereditary afibrinogenemia, and nasal trauma due to a foreign body can also cause epistaxis. Rubeola may cause an oozing nosebleed along with the characteristic maculopapular rash. Two rare childhood diseases — pertussis and diphtheria — can

also cause oozing epistaxis.

Suspect a bleeding disorder if you see excess umbilical cord bleeding at birth or profuse bleeding during circumcision. Epistaxis commonly begins at puberty in patients with hereditary hemorrhagic telangiectasia.

Geriatric Pointers

Elderly patients are more likely to have posterior nosebleeds.

REFERENCES

Camp, A. A. , Dutton, J. M., & Caldarelli, D. D. (2009) . Endoscopic transnasal transethmoid ligation of the anterior ethmoid artery.

American Journal of Rhinologic Allergy, 23, 200–202.

Dallan, I., Tschabitscher, M., Castelnuovo, P., Bignami, M., Muscatello, L., Lenzi, R., … Sellari-Franceschini, S. (2009). Management of severely bleeding ethmoidal arteries. Journal of Craniofacial Surgery, 20, 450–454.

Erythema

[Erythroderma]

Dilated or congested blood vessels produce red scaly skin, or erythema, the most common sign of skin inflammation or irritation. Erythema may be localized or generalized and may occur suddenly or gradually. Skin color can range from bright red in patients with acute conditions to pale violet or brown in those with chronic problems. Erythema must be differentiated from purpura, which causes redness from bleeding into the skin. When pressure is applied directly to the skin, erythema blanches momentarily, but purpura doesn’t.

Erythema usually results from changes in the arteries, veins, and small vessels that lead to increased small-vessel perfusion. Drugs and neurogenic mechanisms can allow extra blood to enter the small vessels. Erythema can also result from trauma and tissue damage; changes in supporting tissues, which increase vessel visibility; and many rare disorders. (See Rare Causes of Erythema.)

Rare Causes of Erythema

In exceptional cases, the patient’s erythema may be caused by one of these rare disorders:

Acute febrile neutrophilic dermatosis, which produces erythematous lesions on the face, neck, and extremities after a high fever.

Erythema ab igne, which produces lacy erythema and telangiectases after exposure to radiant heat.

Erythema chronicum migrans, which produces erythematous macules and papules on the trunk, upper arms, or thighs after a tick bite.

Erythema gyratum repens, which produces wavy bands of erythema and is commonly associated with internal malignancy.

Toxic epidermal necrolysis, which causes severe, widespread erythema, tenderness, bullae formation, and exfoliation, is most commonly caused by medications and may be fatal due

to epidermal destruction and its consequences.

EMERGENCY INTERVENTIONS

If the patient has sudden progressive erythema with a rapid pulse, dyspnea, hoarseness, and agitation, quickly take his vital signs. These may be indications of anaphylactic shock. Provide emergency respiratory support and give epinephrine.

History and Physical Examination

If erythema isn’t associated with anaphylaxis, obtain a detailed health history. Find out how long the patient has had the erythema and where it first began. Has he had associated pain or itching? Has he recently had a fever, upper respiratory tract infection, or joint pain? Does he have a history of skin disease or other illness? Does he or anyone in his family have allergies, asthma, or eczema? Find out if he has been exposed to someone who has had a similar rash or who’s now ill. Did he have a recent fall or injury in the area of erythema?

Obtain a complete drug history, including recent immunizations and over-the-counter drugs. Ask about food intake and exposure to chemicals.

Begin the physical examination by assessing the extent, distribution, and intensity of erythema. Look for hair loss, edema, and other skin lesions, such as hives, scales, papules, and purpura. Examine the affected area for warmth, and gently palpate it to check for tenderness or crepitus.

CULTURAL CUE

Recognizing erythema in patients with darker skin tones may be more challenging. They may present with areas of persistent redness with blue or purple hues, while lighter skinned patients may present with persistent areas of redness only.

Medical Causes

Allergic reactions. Foods, drugs, chemicals, and other allergens can cause an allergic reaction and erythema. A localized allergic reaction also produces hivelike eruptions and edema. Anaphylaxis, a life-threatening condition, produces relatively sudden erythema in the form of urticaria. It also produces flushing; facial edema; diaphoresis; weakness; sneezing; bronchospasm with dyspnea and tachypnea; shock with hypotension and cool, clammy skin; and, possibly, airway edema with hoarseness and stridor.

Burns. With thermal burns, erythema and swelling appear first, possibly followed by deep or superficial blisters and other signs of damage that vary with the burn’s severity. Burns from ultraviolet rays, such as sunburn, cause delayed erythema and tenderness on exposed areas of the skin.

Candidiasis. When candidiasis — a fungal infection — affects the skin, it produces erythema and a scaly, papular rash under the breasts and at the axillae, neck, umbilicus, and groin, also

known as intertrigo. Small pustules commonly occur at the periphery of the rash (satellite pustulosis).

Cellulitis. Erythema, tenderness, and edema are a result of a bacterial infection of the skin and subcutaneous tissue.

Dermatitis. Erythema commonly occurs in this family of inflammatory disorders. With atopic dermatitis, erythema and intense pruritus precede the development of small papules that may redden, weep, scale, and lichenify. These occur most commonly at skin folds of the extremities, neck, and eyelids.

Contact dermatitis occurs after exposure to an irritant. It quickly produces erythema and vesicles, blisters, or ulcerations on exposed skin.

With seborrheic dermatitis, erythema appears with dull red or yellow lesions. Sharply marginated, these lesions are sometimes ring shaped and covered with greasy scales. They usually occur on the scalp, eyebrows, ears, and nasolabial folds, but they may form a butterfly rash on the face or move to the chest or to skin folds on the trunk. This disorder is common in patients infected with human immunodeficiency virus and in infants (cradle cap).

Dermatomyositis. Dermatomyositis, most common in women older than age 50, produces a dusky lilac rash on the face, neck, upper torso, and nail beds. Gottron’s papules (violet, flattopped lesions) may appear on finger joints.

Erythema annulare centrifugum. Small, pink infiltrated papules appear on the trunk, buttocks, and inner thighs, slowly spreading at the margins and clearing in the center. Itching, scaling, and tissue hardening may occur.

Erythema marginatum rheumaticum. Associated with rheumatic fever, erythema marginatum rheumaticum causes erythematous lesions that are superficial, flat, and slightly hardened. They shift, spread rapidly, and may last for hours or days, recurring after a time.

Erythema multiforme. Erythema multiforme is an acute inflammatory skin disease that develops as a result of drug sensitivity after infection, most commonly herpes simplex and Mycoplasma; allergies; and pregnancy. One-half of the cases are of idiopathic origin.

Erythema multiforme minor has typical urticarial red-pink iris-shaped localized lesions with little or no mucous membrane involvement. Most lesions occur on flexor surfaces of the extremities. Burning or itching may occur before or in conjunction with lesion development. Lesions appear in crops and last 2 to 3 weeks. After 1 week, individual lesions become flat or hyperpigmented. Early signs and symptoms may include a mild fever, cough, and sore throat.

Erythema multiforme major usually occurs as a drug reaction; has widespread symmetrical, bullous lesions that may become confluent; and includes erosions of the mucous membranes. Erythema is characteristically preceded by blisters on the lips, tongue, and buccal mucosa and a sore throat. Additional signs and symptoms that manifest early in the course of the disease include a cough, vomiting, diarrhea, coryza, and epistaxis. Later signs and symptoms include a fever, prostration, difficulty with oral intake due to mouth and lip lesions, conjunctivitis due to ulceration, vulvitis, and balanitis. The maximal variant of this disease is considered by many to be Stevens-Johnson syndrome, a multisystem disorder that can occasionally be fatal. In addition to all signs and symptoms mentioned above, the patient develops exfoliation of the skin from disruptions of bullae, although less than 10% of the body surface area is affected. These areas resemble second-degree thermal burns and should be cared for as such. Fever may rise to 102°F to 104°F (38.9°C to 40°C). The patient may also experience tachypnea; a weak, rapid pulse; chest pain; malaise; and muscle or joint pain.

Radiation and other treatments. Radiation therapy may produce dull erythema and edema within 24 hours. As the erythema fades, the skin becomes light brown and mildly scaly. Any treatment that causes an allergic reaction can also cause erythema.

Special Considerations

Because erythema can cause fluid loss, closely monitor and replace fluids and electrolytes, especially in patients with burns or widespread erythema. Make sure to withhold all medications until the cause of the erythema has been identified. Then expect to administer an antibiotic and a topical or systemic corticosteroid.

Drugs Associated with Erythema

There are more than 60 drugs known to cause erythema. Some of the more common instigators are listed below:

Suspect drug-induced erythema in a patient who develops this sign within 1 week of starting a drug. Erythematous lesions can vary in size, shape, type, and amount, but they almost always appear suddenly and symmetrically on the trunk and inner arms.

Some drugs — particularly barbiturates, hormonal contraceptives, salicylates, sulfonamides, and tetracycline — can cause a “fixed” drug eruption. In this type of reaction, lesions can appear on any body part and flake off after a few days, leaving a brownish purple pigmentation. Repeated drug administration causes the original lesions to recur and new ones to develop.

For the patient with itching skin, instruct him to avoid scratching and expect to give soothing baths or to apply open wet dressings containing starch, bran, or sodium bicarbonate; also administer an antihistamine and analgesic as needed. Advise a patient with leg erythema to keep his legs elevated above heart level. For a burn patient with erythema, immerse the affected area in cold water, or apply a sheet soaked in cold water to reduce pain, edema, and erythema. For a patient who is on long-term bed rest, reposition him as ordered, check the skin for areas of pressure-induced erythema (stage 1 ulcer), and provide relief by using special foam cushions.