Edema and Related Medical Conditions

Comprehensive information on edema, swelling, treatment and medical conditions that can cause edema. For all articles, please click on "Archives"

Sunday, July 30, 2006

Angioedema of the Tongue

Angioedema of the Tongue - A Review of Articles and Abstracts

* * * * *

Angioedema of the Tongue
Volume 355:295

July 20, 2006
Number 3

A 75-year-old man presented to the emergency department with diffuse swelling of his tongue that had begun a few hours earlier. He had no known history of allergies. He had been taking 25 mg of captopril twice daily for the past three years because of hypertension. On examination, he could neither speak nor swallow. He had a large, swollen, protuberant tongue (Panels A and B) and hypersalivation and was breathing through his nose. His blood pressure was normal. He had mild tachypnea, but not hypoxemia, stridor, or wheezing. Angioedema was diagnosed, and the patient was treated with epinephrine, antihistamines, and corticosteroids; the symptoms resolved over a three-hour period. Laboratory tests subsequently showed that tryptase and complement component levels (C1q, C3, and C4) were normal. The angioedema was likely due to the angiotensin-converting–enzyme inhibitor.


* * * *

Tongue swelling in the recovery room: a case report and discussion of postoperative angioedema.

May 19 2006

Reed LK,
Meng J,
Joshi GP.

Department of Anesthesiology and Pain Management, University of Texas Southwestern Medical Center at Dallas, 75390-9068, USA.

We present a case of potentially life-threatening postoperative swelling of the tongue and oropharynx that developed in the postanesthesia care unit in a patient taking lisinopril. The principal treatment of angioedema is the discontinuation of the precipitating agent and airway management. Patients with swelling limited to the face and oral cavity may only require monitoring. However, those with swelling in the floor of the mouth, tongue, and supraglottic or glottic areas should have their airway secured by tracheal intubation immediately. Early intubation in patients displaying these characteristics may decrease the incidence of emergent surgical airways. Angioedema is self-limiting, and the swelling usually resolves spontaneously in two to 3 days. Proper identification of angiotensin-converting enzyme inhibitor-associated angioedema requiring a timely airway intervention may reduce mortality, and recognition of its self-limiting course can prevent unnecessary tracheostomy.

PMID: 16731329 [PubMed - in process]

* * * * *

Life-threatening orolingual angioedema during thrombolysis in acute ischemic stroke.

Oct 2005

Engelter ST,
Fluri F,
Buitrago-Tellez C,
Marsch S,
Steck AJ,
Ruegg S,
Lyrer PA.

Neurological Clinic and Stroke Unit, University Hospital Basel, Petersgraben 4, 4031 Basel, Switzerland.

BACKGROUND: Orolingual angioedema can occur during thrombolysis with alteplase in stroke patients. However, data about its frequency, severity and the significance of concurrent use of angiotensin-converting-enzyme inhibitors (ACEi) are sparse.

OBJECTIVE: (1), to alert to the potentially life-threatening complication of orolingual angioedema. (2), to present CT-scans of the tongue which exclude lingual hematoma. (3), to estimate the frequency of orolingual angioedema. (4), to evaluate the risk associated with the concurrent use of ACEi.

METHODS: Single center, databank-based observational study on 120 consecutive patients with i. v. alteplase for acute stroke. Meta-analysis of all stroke studies on alteplase-associated angioedema, which provided detailed information about the use of ACE-inhibitors. Across studies, the Peto odds ratio of orolingual angioedema for "concurrent use of ACEi" was calculated.

RESULTS: Orolingual angioedema occurred in 2 of 120 patients (1.7%, 95% CI 0.2-5.9 %).Angioedema was mild in one, but rapidly progressive in another patient. Impending asphyxia prompted immediate intubation. CT showed orolingual swelling but no bleeding. One of 19 (5%) patients taking ACEi had orolingual angioedema, compared to 1 of 101 (1%) patients without ACEi. Medline search identified one further study about the occurrence of alteplase-associated angioedema in stroke patients stratified to the use of ACEi. Peto odds ratio of 37 (95 % CI 8-171) indicated an increased risk of alteplasetriggered angioedema for patients with ACEi (p <0.001).>

CONCLUSION: Orolingual angioedema is a potentially life-threatening complication of alteplase treatment in stroke patients, especially in those with ACEi. Orolingual hematoma as differential diagnosis can be excluded by CT-scan.

PMID: 16184341 [PubMed - indexed for MEDLINE]

* * * *

Airway compromise due to angiotensin-converting enzyme inhibitor-induced angioedema: clinical experience at a large community teaching hospital.

Laryngeal edema and death from asphyxiation after tooth extraction in four patients with hereditary angioedema.

Tongue angioedema associated with angiotensin-converting enzyme inhibitor (diagnosis, differential diagnosis, treatment)

Sunday, July 23, 2006

Cardiopulmonary Function After Recovery From Swimming-induced Pulmonary Edema.

Cardiopulmonary Function After Recovery From Swimming-induced Pulmonary Edema.

Journal of Sports Medicine

July 16, 2006

Ludwig BB,
Mahon RT,
Schwartzman EL.

*National Naval Medical Center, Division of Pulmonary and Critical Care, Bethesda, MD daggerNaval Medical Research Center, Undersea Medicine Department, Silver Spring, MD double daggerNaval Medical Center Portsmouth, Division of Cardiology, Portsmouth, VA.


This study aimed to compare cardiopulmonary function in patients with a history of swimming-induced pulmonary edema (SIPE) with controls by measuring pulmonary function tests, oxygen consumption with exercise, and the pulmonary arterial pressure response to hypoxemia. DESIGN: Case control study.


Tertiary Military Medical Center.


US Navy Special Warfare members who had previously suffered SIPE.


Measurement of pulmonary function tests, cardiopulmonary exercise test, pulmonary artery pressure by echocardiography at rest on room air and with hypoxia.


Pulmonary function testing, carbon monoxide diffusing capacity, maximal oxygen consumption, and pulmonary arterial pressure response to hypoxemia. RESULTS: Subjects who previously had SIPE did not demonstrate differences in pulmonary function tests, carbon monoxide diffusing capacity, maximal oxygen consumption, or pulmonary arterial pressure response to hypoxemia.


Subjects with a history of SIPE do not have abnormal pulmonary function tests, abnormal exercise capacity, or abnormal pulmonary arterial pressure response to hypoxemia when tested in dry conditions.

PMID: 16858220 [PubMed - as supplied by publisher]

Sunday, July 16, 2006

Chronic edema

Chronic edema

What is Chronic edema?

Chronic edema is swelling that results when, over time, fluid seeps from small blood vessels (capillaries) into body tissues. Normally, fluid passes from the capillaries into the tissues, then back through the vessel walls into the circulation. Nutrients and oxygen in the blood remain in the cells, and waste products are removed. Edema results when fluid does not return in normal amounts from the cells to the bloodstream to continue its flow back to the heart. This may happen at any point in the blood’s circulation, although edema is most common in the lower legs, ankles, and feet. A person may notice swelling, or the collection of fluid may not be obvious. Weight gain may be a symptom.

Possible causes

Several conditions can cause edema. One is heart failure, in which a weakened heart does not pump blood effectively. It is less able to push fluid through the body, and as a result fluid backs up. The pressure that builds up in the blood vessel forces fluid into the tissues and does not permit it to easily pass out through the capillary walls. A clot or tumor in a blood vessel may also cause this buildup of pressure.

Kidney (renal) failure can also cause edema. The kidneys normally play an active role in the flow of fluid between tissues and capillaries. One function of the kidneys is to pass excess salt from the body in the urine. In kidney failure, salt collects in body tissues and attracts fluid (water).

Among the other conditions that can cause chronic edema are poor nutrition and liver disease, in which an abnormal loss of protein disrupts the flow of fluid from the body’s tissues. (Swelling that occurs during the menstrual cycle or following an injury is not chronic edema.)

Getting help

It may be helpful for a woman to limit fluid and salt intake, exercise by walking in place, avoid standing for long periods, and elevate her legs when sitting. Thigh-high elastic stockings may also relieve swelling. Check with your doctor to ensure the safety of any of these acts.

Published: Jul/Aug 2001

Women's Health Monitor

Sunday, July 09, 2006

Hives and Angioedema overview

Hives and Angioedema overview

Mayo Clinic


Hives — also known as urticaria — are raised, red, often itchy welts (wheals) of various sizes that appear and disappear on the skin. Angioedema, a similar swelling, causes large welts deeper in the skin, especially near the eyes and lips. A more serious condition — hereditary angioedema (HAE) — is an uncommon, inherited disorder, which can cause sudden, severe and rapid swelling of the face, arms, legs, hands, feet, genitalia, digestive tract and airway.

As many as one in five people experiences acute hives or angioedema at one time or another. HAE affects only about 6,000 people in the United States.

In most cases, hives and angioedema are harmless and leave no lasting marks. The common treatment is medications. Serious angioedema can be life-threatening if swelling causes your throat or tongue to block your airway and leads to loss of consciousness.

Signs and Symptoms

Acute hives can last from less than a day to up to six weeks, whereas chronic hives last more than six weeks — sometimes occurring for months to years at a time. Often, angioedema and hives occur at the same time.

Hives are raised, red bumps of various sizes that appear and disappear on your skin. They're often itchy and may look similar to mosquito bites. Wheals tend to occur in batches.

Angioedema is similar to hives, but occurs deeper in the skin. Signs and symptoms of angioedema include large welts or swelling of the skin that may occur in the following locations:

Especially near your eyes and lips
On your hands
On your feet

On your genitalia
Inside your throat

Signs and symptoms of HAE include:

Sudden and severe swelling of your face, arms, legs, hands, feet, genitalia, digestive tract and airway
Abdominal cramping as a result of digestive tract swelling
Difficulty or obstructed breathing due to swelling of your airway


The lesions of hives and angioedema are caused by inflammation in the skin. In some cases, hives and angioedema are triggered when certain cells (mast cells) — which line the blood vessels in your skin — release histamine and other chemicals into your bloodstream and skin.

Allergic reactions to medications or foods can cause acute hives or angioedema. Many allergens have been identified.

Examples include:

Foods. Many foods can cause problems in sensitive people, but shellfish, fish, nuts, eggs and milk are frequent offenders.

Medications. Almost any medication may cause hives or angioedema, but more common culprits include antibiotics, aspirin, ibuprofen (Advil, Motrin, others) and blood pressure medications.
Other allergens. Other substances that can cause hives and angioedema include pollen, animal dander, latex and substances injected into your skin from insect stings.

Additional triggers that may produce hives or angioedema include:

Physical factors. Environmental elements also can result in the release of histamine with subsequent hives or angioedema in some people. Examples of these factors include elements such as heat, cold, sunlight, water, pressure on the skin, emotional stress and exercise.

Dermatographism. The name of this condition literally means "write on the skin." When pressure is applied to the skin or the skin is scratched, raised lines appear on those areas due to histamine-based angioedema that leads to swelling beneath the skin.

In addition to these triggers, hives and angioedema sometimes may occur in response to the body's production of antibodies. Some examples of situations in which this might occur include blood transfusions, immune system disorders, such as lupus or cancer, certain thyroid disorders and infections, such as hepatitis A or B, or even a cold.

Hereditary angioedema is an inherited form of angioedema and is related to low levels or abnormal functioning of certain blood proteins (C1 inhibitors). These inhibitors play a role in regulating how your immune system functions.

Risk Factors

You may be at greater risk of hives and angioedema if you:
Have had hives or angioedema before
Have had other allergic reactions
Have a family history of hives or angioedema
Have a family history of hereditary angioedema

When to seek medical advice

Mild hives and angioedema usually aren't life-threatening, and often you can treat hives and angioedema at home. However, seek emergency care if you feel lightheaded, have difficulty breathing, or if swelling or hives don't respond to treatment or continue to appear for more than a couple of days.

Screening and diagnosis

It's sometimes impossible to determine the cause of hives or angioedema. Your doctor will begin by asking you about your medical history. This may include asking you to create a detailed diary of exposure to possible irritants. It's important to tell your doctor about all medications you take, including over-the-counter (OTC) drugs and herbal remedies, even if you don't take them every day. Your doctor may also want to conduct allergy tests, such as skin tests.

If your doctor suspects HAE, he or she may ask for blood tests to check for levels and function of specific blood proteins. If your doctor suspects allergy to food, latex, animal dander, pollen or medication, he or she may recommend allergy skin or blood tests.


Hives and angioedema can, at the least, cause itching and discomfort. In more serious cases — when swelling occurs inside your mouth or throat — complications can include difficulty breathing or loss of consciousness. Anaphylactic shock (anaphylaxis) is a serious allergic reaction involving your heart or lungs. Your bronchial tubes narrow, it's difficult to breathe, and your blood pressure drops, causing dizziness and perhaps loss of consciousness or even death. This occurs rapidly, and requires immediate medical care.


If your symptoms are mild, you may not need treatment. The standard treatment for hives and angioedema is antihistamines, which block the symptom-producing release of histamine. These include:

Nonprescription medications

Diphenhydramine (Benadryl, others)
Chlorpheniramine (Chlor-Trimeton, others)
Clemastine (Tavist, others)
Loratadine (Alavert, Claritin)
Antihistamines such as diphenhydramine, chlorpheniramine and clemastine may cause drowsiness. Loratadine usually doesn't cause drowsiness.

Prescription medications

Desloratadine (Clarinex)
Fexofenadine (Allegra)
Cetirizine (Zyrtec)
Hydroxyzine (Atarax, Vistaril)

Occasionally, for severe hives or angioedema, doctors may prescribe an oral corticosteroid drug — such as prednisone — which can help lessen swelling, redness and itching.

Although useful in treating hives and angioedema, these medications are often ineffective in treating hereditary angioedema. Medications used specifically to treat HAE on a long-term basis include certain androgens, such as danazol (Danocrine), that help regulate levels of blood proteins.

For a severe attack of hives or angioedema, you may need an emergency injection of adrenaline (epinephrine) and a trip to the emergency room. If you have repeated attacks, despite treatment, your doctor may prescribe — and instruct you how to use — adrenaline to carry with you for use in emergency situations.


To lower the likelihood of experiencing hives or angioedema, take the following precautions:

Avoid known triggers. These may include certain foods or medications, or situations, such as temperature extremes, that have triggered past allergic attacks.

Keep a diary. If you suspect foods of causing the problem, keep a food diary. Be aware that some foods may contain ingredients that are listed by less common names on the label.


If you're experiencing mild hives or angioedema, these tips may help relieve your symptoms:

Avoid irritating affected areas.
Take cool showers.
Apply cool compresses.
Wear loose, light clothing.
Minimize vigorous activity, which can release more irritants into the skin.
Use over-the-counter antihistamines to help relieve the itching.

Mayo Clinic

Sunday, July 02, 2006

Symptomatic Vasogenic Edema in Arteriovenous Malformations

Symptomatic Vasogenic Edema in Arteriovenous Malformations provides Clues regarding AVM Pathogenesis

Cerebral arteriovenous malformations (AVMs) can cause neurologic symptoms by bleeding or by inducing seizures. Less common but more dramatic is the syndrome of progressive neurologic deterioration caused by an AVM. This syndrome is usually associated with large AVMs and may sometimes be caused by "vascular steal" whereby blood is shunted preferentially through the low resistance channels of the AVM with consequent ischemia in surrounding brain. The vascular steal theory of the etiology of progressive neurologic deterioration finds support in the observation that occluding feeders to the AVM can ameliorate the symptoms. Other mechanisms, however,are likely to play a role in some of these progressive deficits. Obstructive hydrocephalus from ventricular compression by dilated deep veins is one such mechanism that can be readily identified by CT and MRI scans. Venous hypertension from arterialization of the venous system is also a likely cause of symptoms in many patients, as demonstrated in the abiltity of dural AVMs-which draw no blood from the intracranial vasculature-to produce an identical syndrome. Rarely, AVMs may become symptomatic due to mass effect, which has been demonstrated in some large AVMs with no history of hemorrhage but with regions of hypodensity (edema) around the lesion (Fig. 1).

We have recently had experience at the MGH Brain Aneurysm/AVM Center with a number of such patients who presented with progressive neurologic deficits without angiographic evidence of steal or computed tomographic evidence of hemorrhage. In each case, magnetic resonance imaging revealed evidence of mass effect and edema surrounding the AVM nidus. Interestingly, all of the affected patients had radiographic evidence of venous thrombosis effecting the AVM's drainage. Pathophysiologically, venous outflow obstruction appeared to be a prominent feature in these cases as there was angiographic evidence of venous thrombosis in the AVM drainage system in each patient. In addition, the majority of patients presenting with this syndrome had venous ectasias.

In all of the treated cases the edema resolved after successful arterial embolization. Patients were then treated by surgical removal of their AVM or in one case by successful proton beam therapy. Several patients were also treated acutely with anticoagulation because of evidence that venous thrombosis had precipitated their peri-nidal edema and neurologic deterioration.

Implications of venous-thrombosis-induced perinidal-edema regarding AVM pathogenesis

A number of observations suggest that obstruction of the venous drainage of AVMs may be an important cause of hemorrhage, which is the most common cause of AVM-related neurologic symptoms.

First, a small number of draining veins, venous stenosis, and deep venous drainage have all been identified as risk factors for hemorrhage from an AVM. In addition, within gross specimens of AVMs evidence for subacute thrombosis and previous thrombosis of vascular channels may be observed. Finally, AVMs may spontaneously thrombose or transiently decrease in size consistent with partial thrombosis. This usually occurs in association with hemorrhage. All of these factors argue that acute thrombosis of part of an AVM may be a frequent cause of hemorrhage from these lesions.

Alternatively, increase in venous resistance due to progressive thickening might cause an increase in the pressure in the AVM. The absence of elasticity of the AVM coupled with the inability of the feeding vessels to regulate flow (because of the absence of innervation) presumably causes a pressure increase throughout the lesion in response to outflow obstruction (Fig. 2). Such obstruction may then lead to one of three outcomes: edema, hemorrhageif a weak point in the vascular channels cannot withstand the increased pressure, or complete thrombosis of the lesion.


Our recent experience with AVMs presenting with symptomatic cerebral edama and venous occlussion illustrates the importance of acute obstruction of AVM drainage in causing AVM symptoms. It also demonstrates that special considerations and therapies are necessary to successfully treat patients with symptomatic vasogenic edema caused by arteriovenous malformations.


Further discussion of this topic and references to the original medical literature may be found in:
Tatter SB, Ogilvy CS. Vascular malformations. General considerations. In Ojemann RG, Ogilvy CS, Heros RC, Crowell RM, eds. Surgical Management of Cerebrovascular Disease, Third edition. Williams & Wilkins, Baltimore, in press.

Harvard Edu - Massachusetts General Hospital