A bluish or purplish discoloration of the skin and mucous membranes due to an increase in the amount of deoxygenated hemoglobin in the blood or a structural defect in the hemoglobin molecule.
The presence of methemoglobin in the blood, resulting in cyanosis. A small amount of methemoglobin is present in the blood normally, but injury or toxic agents convert a larger proportion of hemoglobin into methemoglobin, which does not function reversibly as an oxygen carrier. Methemoglobinemia may be due to a defect in the enzyme NADH methemoglobin reductase (an autosomal recessive trait) or to an abnormality in hemoglobin M (an autosomal dominant trait). (Dorland, 27th ed)
Symmetrical osteitis of the four limbs, chiefly localized to the phalanges and the terminal epiphyses of the long bones of the forearm and leg, sometimes extending to the proximal ends of the limbs and the flat bones, and accompanied by dorsal kyphosis and joint involvement. It is often secondary to chronic conditions of the lungs and heart. (Dorland, 27th ed)
Diversion of the flow of blood from the entrance to the right atrium directly to the pulmonary arteries, avoiding the right atrium and right ventricle (Dorland, 28th ed). This a permanent procedure often performed to bypass a congenitally deformed right atrium or right ventricle.
Developmental abnormalities involving structures of the heart. These defects are present at birth but may be discovered later in life.
A congenital heart defect characterized by downward or apical displacement of the TRICUSPID VALVE, usually with the septal and posterior leaflets being attached to the wall of the RIGHT VENTRICLE. It is characterized by a huge RIGHT ATRIUM and a small and less effective right ventricle.
Abnormal formation of blood vessels that shunt arterial blood directly into veins without passing through the CAPILLARIES. They usually are crooked, dilated, and with thick vessel walls. A common type is the congenital arteriovenous fistula. The lack of blood flow and oxygen in the capillaries can lead to tissue damage in the affected areas.
A combination of congenital heart defects consisting of four key features including VENTRICULAR SEPTAL DEFECTS; PULMONARY STENOSIS; RIGHT VENTRICULAR HYPERTROPHY; and a dextro-positioned AORTA. In this condition, blood from both ventricles (oxygen-rich and oxygen-poor) is pumped into the body often causing CYANOSIS.
Abnormal thoracoabdominal VISCERA arrangement (visceral heterotaxy) or malformation that involves additional CONGENITAL HEART DEFECTS (e.g., heart isomerism; DEXTROCARDIA) and/or abnormal SPLEEN (e.g., asplenia and polysplenia). Irregularities with the central nervous system, the skeleton and urinary tract are often associated with the syndrome.
A procedure in which total right atrial or total caval blood flow is channeled directly into the pulmonary artery or into a small right ventricle that serves only as a conduit. The principal congenital malformations for which this operation is useful are TRICUSPID ATRESIA and single ventricle with pulmonary stenosis.
The short wide vessel arising from the conus arteriosus of the right ventricle and conveying unaerated blood to the lungs.
A compound consisting of dark green crystals or crystalline powder, having a bronze-like luster. Solutions in water or alcohol have a deep blue color. Methylene blue is used as a bacteriologic stain and as an indicator. It inhibits GUANYLATE CYCLASE, and has been used to treat cyanide poisoning and to lower levels of METHEMOGLOBIN.
The veins that return the oxygenated blood from the lungs to the left atrium of the heart.
The venous trunk which returns blood from the head, neck, upper extremities and chest.
A surface anesthetic that acts by preventing transmission of impulses along NERVE FIBERS and at NERVE ENDINGS.
An infant during the first month after birth.
A FLAVOPROTEIN oxidoreductase that occurs both as a soluble enzyme and a membrane-bound enzyme due to ALTERNATIVE SPLICING of a single mRNA. The soluble form is present mainly in ERYTHROCYTES and is involved in the reduction of METHEMOGLOBIN. The membrane-bound form of the enzyme is found primarily in the ENDOPLASMIC RETICULUM and outer mitochondrial membrane, where it participates in the desaturation of FATTY ACIDS; CHOLESTEROL biosynthesis and drug metabolism. A deficiency in the enzyme can result in METHEMOGLOBINEMIA.
A syndrome characterized by the clinical triad of advanced chronic liver disease, pulmonary vascular dilatations, and reduced arterial oxygenation (HYPOXEMIA) in the absence of intrinsic cardiopulmonary disease. This syndrome is common in the patients with LIVER CIRRHOSIS or portal hypertension (HYPERTENSION, PORTAL).
The pathologic narrowing of the orifice of the PULMONARY VALVE. This lesion restricts blood outflow from the RIGHT VENTRICLE to the PULMONARY ARTERY. When the trileaflet valve is fused into an imperforate membrane, the blockage is complete.
Absence of the orifice between the RIGHT ATRIUM and RIGHT VENTRICLE, with the presence of an atrial defect through which all the systemic venous return reaches the left heart. As a result, there is left ventricular hypertrophy (HYPERTROPHY, LEFT VENTRICULAR) because the right ventricle is absent or not functional.
Developmental abnormalities in any portion of the ATRIAL SEPTUM resulting in abnormal communications between the two upper chambers of the heart. Classification of atrial septal defects is based on location of the communication and types of incomplete fusion of atrial septa with the ENDOCARDIAL CUSHIONS in the fetal heart. They include ostium primum, ostium secundum, sinus venosus, and coronary sinus defects.
Radiography of blood vessels after injection of a contrast medium.
An abnormal direct communication between an artery and a vein without passing through the CAPILLARIES. An A-V fistula usually leads to the formation of a dilated sac-like connection, arteriovenous aneurysm. The locations and size of the shunts determine the degree of effects on the cardiovascular functions such as BLOOD PRESSURE and HEART RATE.
The determination of oxygen-hemoglobin saturation of blood either by withdrawing a sample and passing it through a classical photoelectric oximeter or by electrodes attached to some translucent part of the body like finger, earlobe, or skin fold. It includes non-invasive oxygen monitoring by pulse oximetry.
A congenital cardiovascular malformation in which the AORTA arises entirely from the RIGHT VENTRICLE, and the PULMONARY ARTERY arises from the LEFT VENTRICLE. Consequently, the pulmonary and the systemic circulations are parallel and not sequential, so that the venous return from the peripheral circulation is re-circulated by the right ventricle via aorta to the systemic circulation without being oxygenated in the lungs. This is a potentially lethal form of heart disease in newborns and infants.
Developmental abnormalities in any portion of the VENTRICULAR SEPTUM resulting in abnormal communications between the two lower chambers of the heart. Classification of ventricular septal defects is based on location of the communication, such as perimembranous, inlet, outlet (infundibular), central muscular, marginal muscular, or apical muscular defect.
Procedures in which placement of CARDIAC CATHETERS is performed for therapeutic or diagnostic procedures.

Decreased left ventricular filling pressure 8 months after corrective surgery in a 55-year-old man with tetralogy of Fallot: adaptation for increased preload. (1/188)

A 55-year-old man with tetralogy of Fallot underwent corrective surgery. Left ventricular filling pressure increased markedly with increased left ventricular volume one month after surgery, then decreased over the next 7 months, presumably due to increased left ventricular compliance.  (+info)

Left ventricle to pulmonary artery conduit in treatment of transposition of great arteries, restrictive ventricular septal defect, and acquired pulmonary atresia. (2/188)

Progressive cyanosis after banding of the pulmonary artery in infancy occurred in a child with transposition of the great arteries and a ventricular septal defect, and a Blalock-Taussig shunt operation had to be performed. At the time of correction a segment of pulmonary artery between the left ventricle and the band was found to be completely occluded so that continuity between the left ventricle and the pulmonary artery could not be restored. A Rastelli type of operation was not feasible as the ventricular septal defect was sited low in the muscular septum. Therefore, in addition to Mustard's operation, a Dacron conduit was inserted from the left ventricle to the main pulmonary artery to relieve the obstruction. Postoperative cardiac catheterization with angiocardiography indicated a satisfactory haemodynamic result. The patient remains well 11 months after the operation. This operation, a left ventricle to pulmonary artery conduit, may be used as an alternative procedure in patients with transposition of the great arteries, intact interventricular septum, and obstruction to the left ventricular outflow, if the obstruction cannot be adequately relieved.  (+info)

The myocardial profile of the cytosolic isozymes of creatine kinase is apparently not related to cyanosis in congenital heart disease. (3/188)

BACKGROUND: CKMB, the cardiac-specific heterodimer of cytosolic creatine-kinase (CK), is developmentally and physiologically regulated, tissue hypoxia being a proposed regulator. In patients with cyanotic heart disease the myocardium is perfused with partially saturated blood. We questioned whether the myocardium of cyanotic subjects contains higher proportions of CKMB. MATERIALS AND METHODS: CK activity, the distribution of cytosolic CK isozymes, activity of lactic dehydrogenase (LDH), and tissue protein content were determined in obstructive tissues removed at corrective surgery of patients with congenital heart defects. Cyanotic (n = 13) and acyanotic (n = 12) subjects were compared. RESULTS: In cyanotic and acyanotic patients, CK activity was 8.4 +/- 0.6 and 7.6 +/- 0.6 IU/mg protein and the proportion of CKMB was 21 +/- 1.4 and 22 +/- 2. 0% (mean +/- S.E.M), respectively. In the two groups of patients, the activity related to the B subunit corresponded to the steady-state level of the CKBmRNA. The tissue content of protein and the activities of CK and LDH were similar in cyanotic and acyanotic subjects and increased with the age. CONCLUSIONS: The lack of difference in CKMB distribution between the cyanotic and acyanotic patients may either indicate that hypooxygenation is not a regulator of CK isozyme expression, or may be attributed to the already high proportion of this isozyme in hypertrophied, obstructive tissues. Recruitment of additional CKMB, in the cyanotic hearts, may thus not be required.  (+info)

Controlled study of preschool development after surgery for congenital heart disease. (4/188)

AIM: Research into intellectual impairment among children with congenital heart disease has focused mainly on older children. This study was designed to determine whether previous findings are applicable to preschool children. METHODS: Three groups of children under 31/2 years old were assessed immediately before treatment and 12 months later: a group with congenital heart disease awaiting surgery, another awaiting bone marrow transplantation, and a healthy comparison group. RESULTS: Although the means of the three groups were within the normal range, preoperatively the cardiac and transplant groups showed deficits compared with the healthy controls. Postoperatively, continuing developmental deficits were significant only in the children with cyanotic lesions. CONCLUSIONS: Conclusions about intellectual development in older children with congenital heart disease do not apply to preschool children. Before corrective surgery, chronic illness itself appears to be the predominant influence on development. Postoperatively, cyanotic and acyanotic lesions are associated with different short term outcomes.  (+info)

Malnutrition and growth failure in cyanotic and acyanotic congenital heart disease with and without pulmonary hypertension. (5/188)

AIM: To investigate the effect of several types of congenital heart disease (CHD) on nutrition and growth. PATIENTS AND METHODS: The prevalence of malnutrition and growth failure was investigated in 89 patients with CHD aged 1-45 months. They were grouped according to cardiac diagnosis: group aP (n = 26), acyanotic patients with pulmonary hypertension; group ap (n = 5), acyanotic patients without pulmonary hypertension; group cp (n = 42), cyanotic patients without pulmonary hypertension; and group cP (n = 16), cyanotic patients with pulmonary hypertension. Information on socioeconomic level, parental education status, birth weight and nutrition history, number of siblings, and the timing, quality, and quantity of nutrients ingested during weaning period and at the time of the examination were obtained through interviews with parents. RESULTS: There was no significant difference between groups in terms of parental education status, socioeconomic level, duration of breast feeding, and number of siblings (p > 0.05). Group cP patients ingested fewer nutrients for their age compared to other groups. 37 of the 89 patients were below the 5th centile for both weight and length, and 58 of 89 patients were below the 5th centile for weight. Mild or borderline malnutrition was more common in group aP patients. Most group cp patients were in normal nutritional state, and stunting was more common than wasting. Both moderate to severe malnutrition and failure to thrive were more common in group cP patients. CONCLUSION: Patients with CHD are prone to malnutrition and growth failure. Pulmonary hypertension appears to be the most important factor, and cyanotic patients with pulmonary hypertension are the ones most severely affected. This study shows the additive effects of hypoxia and pulmonary hypertension on nutrition and growth of children with CHD.  (+info)

Use of self expanding stents in stenotic aortopulmonary shunts in adults with complex cyanotic heart disease. (6/188)

OBJECTIVE: To describe the use of self expanding stents in treating long segment stenosis of aortopulmonary shunts (APS) in adults. DESIGN: Clinical records, catheterisation data, cineangiograms, and operation notes of four consecutive patients undergoing stent implantation since December 1994 were studied retrospectively. SETTING: A tertiary referral centre for cardiac disease. SUBJECTS: Four patients underwent cardiac catheterisation because of clinical deterioration. Their age ranged between 23 and 32 years. The underlying diagnosis was complex cyanotic heart disease in all. Three had a stenotic interposition graft, and one had a classic Blalock shunt. RESULTS: There was one technical failure owing to migration of the stent distal to an ostial stenosis. The ability index, resting oxygen saturation, and exercise tolerance improved in the remainder. Their medium term results have been excellent. CONCLUSIONS: This technique may further palliate adult patients with complex congenital heart disease, though the long term patency of stents is unknown.  (+info)

A case of methemoglobinemia after ingestion of an aphrodisiac, later proven as dapsone. (7/188)

Methemoglobin (MetHb) is an oxidation product of hemoglobin in which the sixth coordination position of ferric iron is bound to a water molecule or to a hydroxyl group. The most common cause of acquired MetHb-emia is accidental poisoning which usually is the result of ingestion of water containing nitrates or food containing nitrite, and sometimes the inhalation or ingestion of butyl or amyl nitrite used as an aphrodisiac. We herein report a case of MetHb-emia after ingestion of an aphrodisiac, later identified as dapsone by gas chromatograph/mass selective detector (GC/MSD). A 24-year old male was admitted due to cyanosis after ingestion of a drug purchased as an aphrodisiac. On arterial blood gas analysis, pH was 7.32, PaCO2 26.8 mmHg, PaO2 75.6 mmHg, and bicarbonate 13.9 mmol/L. Initial pulse oxymetry was 89%. With 3 liter of nasal oxygen supplement, oxygen saturation was increased to 90-92%, but cyanosis did not disappear. Despite continuous supplement of oxygen, cyanosis was not improved. On the fifth hospital day, MetHb was 24.9%. Methylene blue was administered (2 mg/kg intravenously) and the patient rapidly improved. We proved the composition of aphrodisiac as dapsone by the method of GC/MSD.  (+info)

Occlusion of azygos vein via direct percutaneous puncture of innominate vein following cavopulmonary anastomosis. (8/188)

A 2-year-10-month-old boy was diagnosed with a complex congenital heart disease: right atrial isomerism, left superior vena cava (LSVC), complete atrioventricular septal defect, secundum type atrial septal defect, transposition of the great arteries with pulmonary atresia, patent ductus arteriosus, absence of a right superior vena cava (RSVC), and dextrocardia. He had received a left Blalock-Taussig (BT) shunt at the age of 3 months and a left bidirectional Glenn shunt one year after BT shunt. Progressive cyanosis was noted after the second operation and cardiac catheterization showed a functional Glenn shunt with an engorged azygos vein, which was inadvertently skipped for ligation. Because of the absence of RSVC, transcatheter occlusion of the azygos vein was performed successfully via direct puncture of the innominate vein.  (+info)

In medicine, cyanosis is often used as an indication of the severity of a patient's condition. For example, a patient with severe cyanosis may have a more serious underlying condition than a patient with mild cyanosis. Additionally, cyanosis can be used to monitor the effectiveness of treatment and to determine when further interventions are necessary.

Cyanosis can be diagnosed through physical examination, blood tests, and other diagnostic procedures such as pulse oximetry or arterial blood gas analysis. Treatment for cyanosis depends on the underlying cause and may include oxygen therapy, medication, or surgical intervention.

In summary, cyanosis is a condition characterized by a bluish discoloration of the skin and mucous membranes due to inadequate oxygenation of the body's tissues. It is an important sign of underlying disease and can be used to assess the severity of a patient's condition and monitor the effectiveness of treatment.

There are several possible causes of methemoglobinemia, including:

1. Exposure to certain medications or chemicals, such as nitrates or aniline dyes.
2. Genetic disorders that affect the production or function of hemoglobin.
3. Infections, such as bacterial infections of the blood or respiratory tract.
4. Poor nutrition or malnutrition.
5. Certain chronic medical conditions, such as sickle cell anemia or thalassemia.

Methemoglobinemia can be diagnosed through a variety of tests, including:

1. Complete blood count (CBC) to measure the levels of methemoglobin in the blood.
2. Blood gas analysis to measure the partial pressure of oxygen and carbon dioxide in the blood.
3. Co-oximetry to measure the levels of methemoglobin and other forms of hemoglobin.
4. Urine tests to check for the presence of abnormal hemoglobin.
5. Genetic testing to identify inherited disorders that may be causing the condition.

Treatment of methemoglobinemia depends on the underlying cause and may include:

1. Administration of oxygen therapy to increase the amount of oxygen in the blood.
2. Use of medications to reduce the levels of methemoglobin and increase the levels of normal hemoglobin.
3. Transfusions of red blood cells to replace abnormal hemoglobin with normal hemoglobin.
4. Management of underlying medical conditions, such as infections or genetic disorders.
5. Dietary changes to address any nutritional deficiencies that may be contributing to the condition.

In severe cases of methemoglobinemia, hospitalization may be necessary to provide oxygen therapy and other treatments. In some cases, patients with methemoglobinemia may require long-term management and follow-up care to prevent complications and manage the underlying cause of the condition.

Symptoms of secondary hypertrophic osteoarthropathy may include:

1. Pain and stiffness in the hands and feet
2. Swelling and redness in the affected joints
3. Thickening and enlargement of the bones in the hands and feet
4. Limited range of motion in the affected joints
5. Warmth and erythema (redness) over the affected joints.

SHOA can be diagnosed through a combination of physical examination, X-rays, and other imaging tests such as CT or MRI scans. Treatment for SHOA may include medications to manage pain and inflammation, as well as surgery to remove any excess bone growth. In some cases, the underlying condition that is causing the bone growth may also be treated.

SHOA is a rare condition, and it is estimated to affect only about 1 in 100,000 people. It can occur at any age but is more common in adults. The exact prevalence of SHOA is not known, as it is often misdiagnosed or underdiagnosed.

Secondary hypertrophic osteoarthropathy is a rare condition that causes excessive growth and thickening of the bones in the hands and feet. It is often associated with other conditions, such as inflammatory diseases or cancers. The exact cause of SHOA is not known, but it is thought to be related to an abnormal response to injury or inflammation. Treatment for SHOA typically focuses on managing the underlying condition that is causing the bone growth.

SHOA is a rare and often misdiagnosed condition that can cause significant pain and disability. It is important for individuals who are experiencing symptoms of SHOA to seek medical attention to receive an accurate diagnosis and appropriate treatment. With proper treatment, many people with SHOA can experience improvement in their symptoms and quality of life.

Types of congenital heart defects include:

1. Ventricular septal defect (VSD): A hole in the wall between the two lower chambers of the heart, allowing abnormal blood flow.
2. Atrial septal defect (ASD): A hole in the wall between the two upper chambers of the heart, also allowing abnormal blood flow.
3. Tetralogy of Fallot: A combination of four heart defects, including VSD, pulmonary stenosis (narrowing of the pulmonary valve), and abnormal development of the infundibulum (a part of the heart that connects the ventricles to the pulmonary artery).
4. Transposition of the great vessels: A condition in which the aorta and/or pulmonary artery are placed in the wrong position, disrupting blood flow.
5. Hypoplastic left heart syndrome (HLHS): A severe defect in which the left side of the heart is underdeveloped, resulting in insufficient blood flow to the body.
6. Pulmonary atresia: A condition in which the pulmonary valve does not form properly, blocking blood flow to the lungs.
7. Truncus arteriosus: A rare defect in which a single artery instead of two (aorta and pulmonary artery) arises from the heart.
8. Double-outlet right ventricle: A condition in which both the aorta and the pulmonary artery arise from the right ventricle instead of the left ventricle.

Causes of congenital heart defects are not fully understood, but genetics, environmental factors, and viral infections during pregnancy may play a role. Diagnosis is typically made through fetal echocardiography or cardiac ultrasound during pregnancy or after birth. Treatment depends on the type and severity of the defect and may include medication, surgery, or heart transplantation. With advances in medical technology and treatment, many children with congenital heart disease can lead active, healthy lives into adulthood.


The symptoms of Ebstein anomaly can vary depending on the severity of the defect and may include:

* Shortness of breath (dyspnea)
* Fatigue
* Swelling in the legs, feet, or abdomen (edema)
* Pale skin (cyanosis)
* Rapid breathing (tachypnea)
* A blue tint to the skin and mucous membranes (cyanosis)

Ebstein anomaly can be diagnosed through a variety of tests, including:

* Echocardiogram: This is a non-invasive test that uses sound waves to create images of the heart. It can help doctors visualize the tricuspid valve and determine the severity of the defect.
* Electrocardiogram (ECG): This test measures the electrical activity of the heart and can detect any abnormal rhythms or arrhythmias that may be associated with Ebstein anomaly.
* Chest X-ray: This test can provide images of the heart and lungs and can help doctors identify any other underlying conditions that may be contributing to the symptoms.
* Cardiac catheterization: This is a minimally invasive test in which a thin, flexible tube (catheter) is inserted into the heart through a vein in the leg. It can provide detailed information about the structure and function of the heart and its vessels.

Treatment for Ebstein anomaly may include:

* Medications to control symptoms such as high blood pressure, heart failure, or arrhythmias
* Surgery to repair or replace the tricuspid valve
* Catheter procedures to close any abnormal openings in the heart or to implant devices such as pacemakers or defibrillators
* In some cases, a heart transplant may be necessary.

Overall, the prognosis for individuals with Ebstein anomaly varies depending on the severity of the defect and the presence of any other underlying conditions. With proper medical care and management, many people with this condition can lead active and fulfilling lives. However, it is important to carefully follow the recommended treatment plan and to attend regular follow-up appointments with a healthcare provider to monitor for any changes or complications.

AVMs are characterized by a tangle of abnormal blood vessels that can cause a variety of symptoms, including:

* Headaches
* Seizures
* Stroke-like episodes
* Neurological deficits such as weakness or numbness
* Vision problems
* Pain

AVMs can be diagnosed through a combination of imaging studies such as CT or MRI scans, and catheter angiography. Treatment options for AVMs include:

* Endovascular embolization, which involves using a catheter to inject materials into the abnormal blood vessels to block them off
* Surgery to remove the AVM
* Radiation therapy to shrink the AVM

The goal of treatment is to prevent bleeding, seizures, and other complications associated with AVMs. In some cases, treatment may not be necessary if the AVM is small and not causing any symptoms. However, in more severe cases, prompt treatment can significantly improve outcomes.

1. Ventricular septal defect (VSD): an opening in the wall between the two lower chambers of the heart, which allows oxygen-poor blood to mix with oxygen-rich blood.
2. Pulmonary stenosis: a narrowing of the pulmonary valve and pulmonary artery, which restricts blood flow to the lungs.
3. Overriding aorta: an aorta that grows over the ventricular septal defect, blocking the flow of oxygen-rich blood from the left ventricle to the rest of the body.
4. Right ventricular hypertrophy: enlargement of the right ventricle due to increased pressure caused by the backflow of blood through the VSD.

These abnormalities combine to reduce the amount of oxygen that reaches the body's tissues, leading to cyanosis (blue discoloration of the skin) and fatigue. Tetralogy of Fallot is usually diagnosed at birth or soon after, and treatment typically involves a combination of medications, surgery, and other interventions to repair the defects and improve blood flow to the body.

The term "heterotaxy" comes from the Greek words "heteros," meaning "different," and "taxis," meaning "arrangement." This condition is also known as situs inversus totalis or "complete reversal of internal organs." Heterotaxy syndrome can be diagnosed through imaging tests such as ultrasound, CT scan, or MRI.

The symptoms of heterotaxy syndrome vary depending on the severity of the condition and the specific organs affected. Common symptoms include difficulty breathing, swallowing, and digesting food, as well as abdominal pain, fatigue, and palpitations. Treatment options for heterotaxy syndrome may include surgery to correct any anatomical abnormalities, medication to manage symptoms, and close monitoring by a healthcare provider.

It is essential to seek medical attention if you or your child experiences any of the above symptoms, especially if they worsen over time. An early diagnosis can help prevent complications and improve the chances of successful treatment.

The exact prevalence of HPS is not well-established, but it is believed to affect approximately 30% to 50% of individuals with cirrhosis. Risk factors for developing HPS include alcohol consumption, viral hepatitis, and non-alcoholic fatty liver disease (NAFLD).

The diagnosis of HPS typically involves a combination of physical examination, imaging studies such as ultrasound or CT scans, and laboratory tests to evaluate liver function. Treatment options for HPS depend on the underlying cause of the condition and may include medications to manage portal hypertension, lung fibrosis, or other complications. In severe cases, liver transplantation may be necessary.

Prognosis for individuals with HPS is generally poor, with a 5-year survival rate of approximately 50%. However, early diagnosis and appropriate management can improve outcomes and reduce the risk of complications.

There are several causes of PVS, including:

1. Congenital heart defects: PVS can be present at birth due to abnormal development of the pulmonary valve or other structures near the valve.
2. Rheumatic fever: This is an inflammatory disease that can damage the heart valves, including the pulmonary valve.
3. Endocarditis: This is an infection of the heart valves, which can cause scarring and narrowing of the pulmonary valve.
4. Heart disease: PVS can be a complication of other heart conditions, such as hypertension or coronary artery disease.
5. Calcification: Over time, deposits of calcium can accumulate on the valve leaflets, causing them to become stiff and narrow.

Symptoms of PVS may include:

1. Shortness of breath (dyspnea)
2. Fatigue or weakness
3. Chest pain (angina)
4. Swelling in the legs, ankles, or feet (edema)
5. Palpitations or irregular heartbeat

If PVS is suspected, a healthcare provider may perform several tests to confirm the diagnosis, including:

1. Echocardiogram: This is an ultrasound test that uses sound waves to create images of the heart and its valves.
2. Cardiac catheterization: A thin tube (catheter) is inserted into a blood vessel in the arm or leg and guided to the heart to measure pressure and oxygen levels in the chambers.
3. Chest X-ray: This test can help identify any enlargement of the heart or lungs that may be indicative of PVS.
4. Electrocardiogram (ECG): This test measures the electrical activity of the heart and can help identify irregular heart rhythms or other signs of PVS.

Treatment for PVS may include:

1. Medications to manage symptoms, such as diuretics to reduce fluid buildup in the body, and ACE inhibitors or beta blockers to lower blood pressure.
2. Lifestyle changes, such as a healthy diet, regular exercise, and stress reduction techniques.
3. Valve repair or replacement surgery: In severe cases of PVS, surgery may be necessary to repair or replace the affected valve.

If you suspect you may have PVS, it is important to seek medical attention as soon as possible to receive an accurate diagnosis and appropriate treatment. With prompt and proper treatment, many people with PVS are able to manage their symptoms and improve their quality of life.

Tricuspid atresia is a rare congenital heart defect that occurs when the tricuspid valve, which separates the right atrium and ventricle, does not develop properly and is absent or very small. This results in poor blood flow from the right atrium to the right ventricle, leading to inadequate oxygenation of the body.

Symptoms:

Children with tricuspid atresia may experience symptoms such as:

* Blue tinge to the skin (cyanosis)
* Shortness of breath
* Fatigue
* Poor feeding and growth
* Rapid breathing
* Pallor (pale skin)

Diagnosis:

Tricuspid atresia is diagnosed through a series of tests, including:

* Physical examination
* Chest X-ray
* Echocardiogram (echo)
* Electrocardiogram (ECG)
* Cardiac catheterization

Treatment:

The treatment for tricuspid atresia usually involves a series of surgeries and catheterizations to improve blood flow and oxygenation to the body. These may include:

* Balloon atrial septostomy: A procedure in which a balloon is inserted through a catheter into the atrial septum to create a hole between the atria to improve blood flow.
* Tricuspid valve replacement: A surgical procedure to replace the tricuspid valve with an artificial valve.
* Intracardiac repair: A surgical procedure to repair any other defects in the heart.

Prognosis:

The prognosis for children with tricuspid atresia varies depending on the severity of the defect and the presence of other congenital heart defects. With appropriate treatment, many children with tricuspid atresia can lead active and healthy lives. However, some may experience ongoing health problems and may require long-term monitoring and care.

The AVF is created by joining a radial or brachial artery to a vein in the forearm or upper arm. The vein is typically a radiocephalic vein, which is a vein that drains blood from the hand and forearm. The fistula is formed by sewing the artery and vein together with a specialized suture material.

Once the AVF is created, it needs time to mature before it can be used for hemodialysis. This process can take several weeks or months, depending on the size of the fistula and the individual patient's healing response. During this time, the patient may need to undergo regular monitoring and testing to ensure that the fistula is functioning properly.

The advantages of an AVF over other types of hemodialysis access include:

1. Improved blood flow: The high-flow path created by the AVF allows for more efficient removal of waste products from the blood.
2. Reduced risk of infection: The connection between the artery and vein is less likely to become infected than other types of hemodialysis access.
3. Longer duration: AVFs can last for several years, providing a reliable and consistent source of hemodialysis access.
4. Improved patient comfort: The fistula is typically located in the arm or forearm, which is less invasive and more comfortable for the patient than other types of hemodialysis access.

However, there are also potential risks and complications associated with AVFs, including:

1. Access failure: The fistula may not mature properly or may become blocked, requiring alternative access methods.
2. Infection: As with any surgical procedure, there is a risk of infection with AVF creation.
3. Steal syndrome: This is a rare complication that occurs when the flow of blood through the fistula interferes with the normal flow of blood through the arm.
4. Thrombosis: The fistula may become occluded due to clotting, which can be treated with thrombolysis or surgical intervention.

In summary, an arteriovenous fistula (AVF) is a type of hemodialysis access that is created by connecting an artery and a vein, providing a high-flow path for hemodialysis. AVFs offer several advantages over other types of hemodialysis access, including improved blood flow, reduced risk of infection, longer duration, and improved patient comfort. However, there are also potential risks and complications associated with AVFs, including access failure, infection, steal syndrome, and thrombosis. Regular monitoring and testing are necessary to ensure that the fistula is functioning properly and to minimize the risk of these complications.

In a normal heart, the aorta arises from the left ventricle and the pulmonary artery arises from the right ventricle. In TGV, the positions of these vessels are reversed, with the aorta arising from the right ventricle and the pulmonary artery arising from the left ventricle. This can lead to a variety of complications, including cyanosis (blue discoloration of the skin), tachycardia (rapid heart rate), and difficulty breathing.

TGV is often diagnosed during infancy or early childhood, and treatment typically involves surgery to repair the defect. In some cases, a procedure called an arterial switch may be performed, in which the aorta and pulmonary artery are surgically reversed to their normal positions. In other cases, a heart transplant may be necessary. With proper treatment, many individuals with TGV can lead active and healthy lives. However, they may require ongoing monitoring and care throughout their lives to manage any potential complications.

There are several types of heart septal defects, including atrial septal defects, ventricular septal defects, and mitral valve defects. Ventricular septal defects are the most common type and occur when there is an abnormal opening in the wall between the right and left ventricles.

Symptoms of heart septal defects can include shortness of breath, fatigue, and swelling in the legs and feet. In some cases, the defect may not cause any symptoms at all until later in life.

Diagnosis of heart septal defects is typically made using echocardiography, electrocardiography (ECG), or chest X-rays. Treatment options vary depending on the severity of the defect and can include medication to manage symptoms, surgery to repair the defect, or catheter procedures to close the opening. In some cases, heart septal defects may be treated with a procedure called balloon atrial septostomy, in which a balloon is inserted through a catheter into the abnormal opening and inflated to close it.

Prognosis for patients with heart septal defects depends on the severity of the defect and the presence of any other congenital heart defects. In general, early diagnosis and treatment can improve outcomes and reduce the risk of complications such as heart failure, arrhythmias, and endocardrial infection.

In summary, heart septal defects, ventricular type, are congenital heart defects that occur when there is an abnormal opening in the wall between the right and left ventricles of the heart. Symptoms can include shortness of breath, fatigue, and swelling in the legs and feet. Diagnosis is typically made using echocardiography, electrocardiography (ECG), or chest X-rays. Treatment options vary depending on the severity of the defect and can include medication, surgery, or catheter procedures. Prognosis is generally good for patients with heart septal defects if they receive early diagnosis and treatment.



... is further classified into central cyanosis vs. peripheral cyanosis. The mechanism behind cyanosis is different ... It causes cyanosis even at low blood levels. Peripheral cyanosis is the blue tint in fingers or extremities, due to an ... Peripheral cyanosis may be due to the following causes: All common causes of central cyanosis Reduced cardiac output (e.g. ... Cyanosis may be more difficult to detect on people with darker skin pigmentation. However, cyanosis can still be diagnosed with ...
... cyanosis; increased respiration; nausea; drowsiness; headache; and vomiting. "1-Octanethiol". Sigma-Aldrich. "L07195 1- ...
Thirteen more cases of an unknown disease were admitted, all of whom developed cyanosis and hemoptysis, or bloody sputum, the ... Adeyinka, Adebayo; Kondamundi, Noah P. (September 22, 2020). "Cyanosis". National Center for Biotechnology Information ...
She directed a short, animated documentary during her research in 2007 called Cyanosis, which showed the work of a Tehran ... "Cyanosis , IDFA". Retrieved 2016-05-03. "Rokhsareh Ghaemmaghami". IMDb. Retrieved 2016-05-03. "Afghanistan Series: Online Film ... Ghaemmaghami, Rokhsareh (2000-01-01), Cyanosis, retrieved 2016-05-03 "Going Up the Stairs, a film by Rokhsareh Ghaem Maghami". ... Cyanosis, Documentary with animation, 32 Min., Iran, 2007 Best student Documentary in Sheffield doc/ fest, UK, 2008 Silver ...
While severe cyanosis can be easily noticed, an oxygen saturation as low as 80% causes only mild clinical cyanosis that is ... Babies with cyanosis due to methemoglobinemia also usually present with cyanosis in the neonatal period, but pulse oximetry may ... In contrast, peripheral cyanosis typically has a blueish discoloration over the extremities. Cyanosis can be noted in babies ... Babies with cyanosis due to congenital heart disease usually present with symptoms hours to days after birth. In addition to ...
Cyanosis is typically classified as having 85% or less oxygen saturation in your bloodstream. Typically your blood oxygen ... Lastly, a 25-year-old female had experienced several years of cyanosis and heart palpitations. The individual underwent ... Symptoms of Raghib syndrome include: Heart palpitation Bluish discoloration of the skin (cyanosis) Left-handed clumsiness ... Adeyinka, Adebayo; Kondamudi, Noah (Jan 2022). Cyanosis. Treasure Island (FL): StatPearls Publishing. PMID 29489181. Retrieved ...
... cyanosis occurred; historian Douglas Gill, and the British Army transit camp at Étaples, a possible source of the outbreak, ...
... cyanosis (late sign); increased heart rate. It is a common misconception and pure speculation that atelectasis causes fever. A ...
There seemed to have been an onset of auricular fibrillation . . . extreme cyanosis developed. Massage over the heart was ...
They include fever of 38 °C (100.4 °F) or above; chills; fatigue; bluish skin coloration (cyanosis); sore throat; hoarseness; ...
This may result in the clinical finding of cyanosis, the presence of bluish-colored skin, especially of the lips and under the ... This causes signs of cyanosis.[citation needed] Heart of human embryo of about 35 days Atrial septal defect with left-to-right ...
Eisenmenger syndrome can result in cyanosis. A medical provider (e.g. doctor) may order tests for further evaluation of a heart ... The lack of oxygenation in the pulmonary circulation results in cyanosis. Widely split fixed S2 and systolic ejection murmur at ... Pulmonary hypertension will increase the murmur intensity and may present with cyanosis. Flow murmur presents at the right ... This does not produce cyanosis, but causes pulmonary hypertension. Longstanding uncorrected atrial septal defects can also ...
Signs include cyanosis and exercise intolerance. Polycythemia is often present and, if severe, needs to be controlled with ... cyanosis, and exercise intolerance. Trapped Neutrophil Syndrome* is an autosomal recessive disease which results in mature ...
Cyanosis Mild fever retrosternal chest pain. The condition follows an exposure to breathing through apparatus that could allow ...
for 1861-62 A case of cyanosis. 1862 A case of diseased spleen. 1863 On the use of chlorate of potass. 1863 An account of a ...
Early cyanosis is a symptom of a right-to-left shunt. A right-to-left shunt results in decreased blood flow through the ... minimal cyanosis) Transposition of great vessels Tricuspid atresia Tetralogy of Fallot Total anomalous pulmonary venous return ... resulting in decreased oxygenation of blood and cyanosis. The most common cause of right-to-left shunt is the Tetralogy of ... minimal cyanosis) 2 Vessels involved: Transposition of great vessels 3 Leaflets: Tricuspid atresia 4 Tetra- prefix: Tetralogy ...
Cyanosis or blue skin coloration, primarily affecting the lips and fingernails, can indicate a systemic or circulatory issue. ... This contributes to cyanosis and pulmonary hypertension. For proper diagnosis of situs ambiguus, cardiac and non-cardiac ... Infants who experience severe cyanosis at birth may die within hours of delivery if medical intervention is not immediate. ... contributing to cyanosis and possible respiratory distress. Poor systemic circulation also results due to improper positioning ...
Infants with alpha- or gamma-chain variants manifest cyanosis since birth but transient neonatal cyanosis caused by gamma-chain ... samples to pure oxygen can be used to differentiate cyanosis caused by metHb from cardiopulmonary cyanosis or other cyanosis ... Cyanosis is the most common sign of hemoglobin M disease, which can be observed in all kinds of hemoglobin M diseases. It is ... Cyanosis caused by hemoglobin M disease is often mistaken as cardiac or pulmonary defects. Correct diagnosis is important to ...
Cyanosis: Bluish discoloration of skin while feeding. Weak crying Facial weakness Aspiration Headaches aggravated by Valsalva ...
It causes cyanosis even at low blood levels. It is a rare blood condition in which the β-pyrrole ring of the hemoglobin ... Symptoms include a blueish or greenish coloration of the blood (cyanosis), skin, and mucous membranes, even though a blood ...
Severely affected pets may develop apnea, syncope, cyanosis. In extreme cases, the animal may be exercise intolerant and may ...
Delayed pulmonary edema, cyanosis or bronchopneumonia may develop. The smoke and the spent canisters contain suspected ... the worst cases developing marked dyspnoea and cyanosis leading to death. Respirators are required for people coming into ...
... cyanosis) from lack of oxygen if breathing is not restored. Cyanosis may also be seen on the fingertips.[citation needed] ...
Delayed pulmonary edema, cyanosis or bronchopneumonia may develop. The smoke and the spent canisters contain suspected ... Severe cases can suffer of reduced pulmonary function for some months, the worst cases developing marked dyspnea and cyanosis ...
While crying, oral ventilation occurs and cyanosis subsides. There is variation in the length of time until a baby begins oral ... In these cases there are cyclical periods of cyanosis. The infant initially attempts to breathe through the nose, and is unable ...
The former can be indicated through wheezing and cyanosis. Poor blood circulation leads to a weak pulse, pale skin and fainting ...
Closing of the ductus arteriosus in a heart that is severely underdeveloped on the left results in cyanosis and respiratory ... Early signs and symptoms include poor feeding, cyanosis, and diminished pulse in the extremities. The etiology is believed to ... Early symptoms might include poor feeding or cyanosis that does not respond to oxygen administration. Peripheral pulses may be ... These neonates quickly decompensate and develop acidosis and cyanosis. On EKG, right axis deviation and right ventricular ...
Hypoxemia due to low SaO2 is indicated by cyanosis. Oxygen saturation can be measured in different tissues: Venous oxygen ... Hypoxia due to low SaO2 is indicated by cyanosis, but oxygen saturation does not directly reflect tissue oxygenation. The ...
Cyanosis Headache Decreased reaction time, disorientation, and uncoordinated movement. Impaired judgment, confusion, memory ... hypoxia can result in cyanosis, a blue discoloration of the skin. If hypoxia is very severe, a tissue may eventually become ... and pulmonary hypertension eventually leading to the late signs cyanosis, slow heart rate, cor pulmonale, and low blood ...
Symptoms of exposure include dizziness, headaches, syncope, and cyanosis. Exposure to toxic levels causes severe respiratory ...
Most cyanosis is seen as a result of congenital heart disease, pulmonary disease, or as a terminal ... Lack of oxygen in the blood causes a bluish discoloration in the skin or mucous membranes called cyanosis. ... Lack of oxygen in the blood causes a bluish discoloration in the skin or mucous membranes called cyanosis. Most cyanosis is ...
Cyanosis and Clubbing. Cyanosis. The distinctive blue or purple skin discoloration of cyanosis indicates the presence of at ... Severely anemic patients (regardless of the degree of desaturation) are, therefore, unable to manifest cyanosis. Cyanosis may ... not to the observed anatomic location of the cyanosis. Central cyanosis is often a manifestation of congenital heart disease ... Central cyanosis typically involves the entire body but may be best appreciated on warm areas of the body (eg, tongue, oral ...
An author and heart surgeon, Dr.Mani writes and sells ebooks to raise money that sponsors life-saving operations for children born with heart defects. You can help turn this effort into a movement that transforms many more little lives. Thank you for your support.. ...
irritation skin, mucous membrane; liver damage, jaundice; cyanosis; sneezing; cough, sore throat; peripheral neuropathy, muscle ...
Cyanosis, convulsions, 6-10 6.1 Mice (wn) ip 0.06 Agonal paralysis 6-10 5.0 ...
... cyanosis, inability to drink, or convulsion], or hospitalization) (6). We report the effects of this strategy on a case-series ... cyanosis; inability to drink; or convulsion) or 2 minor signs (i.e., cough, rhinorrhea, sore throat, muscle/joint pain, chills ...
Information on terrorism and public health. Provided by the Centers for Disease Control and Prevention (CDC).
cyanosis,. *fever,. *tachycardia, and. *nausea.. Depending on the extent of exposure, sustained fever and noncardiac pulmonary ...
... cyanosis; and diminished breath sounds. ...
Color changes, cyanosis *Respiratory pauses *Irregular respirations Responses to Tactile Input Oral Reflexes: Oral reflexes can ... If cyanosis is noted it is recommended that the infant be fed with an oximeter in place. A lack of color change with feeding, ... Many infants can have relatively low oxygen saturation without external evidence such as cyanosis. ... but longer periods or those associated with cyanosis, pallor, or bradycardia are pathologic. *Sounds of respirations. Noise ...
Progressive cyanosis following Kawashima operation: slow resolution after redirection of hepatic veins. Journal of ... Progressive cyanosis following Kawashima operation : slow resolution after redirection of hepatic veins. In: Journal of ... Progressive cyanosis following Kawashima operation : slow resolution after redirection of hepatic veins. / Larsen, Signe Holm; ... Larsen, S. H., Emmertsen, K., Bjerre, J., & Hjortdal, V. E. (2013). Progressive cyanosis following Kawashima operation: slow ...
Bluish lips/skin (cyanosis). Keep track of your symptoms and the calendar.. ...
5. Cardiovascular evaluation: a. Cyanosis: Record definite cyanosis which is thought to be related to generalized hemoglobin ... Check especially for cyanosis and venous distention. Check the peripheral pulses-- note the character of the artery as well as ... Cyanosis 1 yes 51 blank 20,271 576 Irregular pulse 1 yes 415 blank 19,907 577 Blank 20,322 578 Neck vein distension 1 yes 53 ...
They experienced yellow hands, cyanosis of the lips and nailbeds, headache, dizziness, nausea, chest pain, confusion and ... a followup study was performed to check workers for signs of cyanosis or other pertinent adverse health effects. Methemoglobin ...
Cyanosis, or a blue tinge to the lips or skin. *Needing to adjust positions in order to breathe (such as sitting up or standing ... cyanosis). This is a medical emergency, and you should call 911 immediately. ...
The second was a 16-month-old girl who started crying and who developed widespread erythema, cyanosis, decreased respiration, ... The first was an 18-month-old boy who developed bradycardia, cyanosis, periorbital edema, widespread erythema, and hypotonia 5 ... two of the patients also had cyanosis. ...
Cyanosis may be present in severe cases. Capnography may be useful in the evaluation of children with potential respiratory ...
Respiratory depression, cyanosis, shock, vomiting, hyperpyrexia, mydriasis, and oliguria or anuria may also be present. ...
Pale gray or blue skin or lips (cyanosis). *Swelling in the legs, belly area or areas around the eyes ...
bluish discoloration of the digits or lips (cyanosis). Specifically, people experiencing septic shock will also have very low ...
Carbaryl is a colorless to white or gray, odorless solid, depending on the purity of the compound. It is used as ...
Cyanosis (blue color of the skin). *Abnormal chest development, with one side being larger than the other ...
Information on terrorism and public health. Provided by the Centers for Disease Control and Prevention (CDC).
Babies will have bluish skin (cyanosis) after the first 2 surgeries, or until the final Fontan procedure is done. Your child ...
Peripheral vascular disease: Decreased peripheral pulses, peripheral arterial bruits, pallor, peripheral cyanosis, gangrene, ... Atheroembolism: Livedo reticularis, gangrene, cyanosis, ulceration, digital necrosis, GI bleeding, retinal ischemia, cerebral ... Peripheral vascular disease - Decreased peripheral pulses, peripheral arterial bruits, pallor, peripheral cyanosis, gangrene, ... Atheroembolism - Livedo reticularis, gangrene, cyanosis, ulceration, digital necrosis, gastrointestinal bleeding, retinal ...
The main symptom of cyanosis is a bluish color of the lips, fingers, and toes that is caused by the low oxygen content in the ... Heart valve defects that can cause cyanosis include:. *Tricuspid valve (the valve between the 2 chambers on the right side of ... It is classified as a cyanotic heart defect because the condition leads to cyanosis, a bluish-purple coloration to the skin, ... Physical examination confirms cyanosis. Older children may have clubbed fingers.. The doctor will listen to the heart and lungs ...
2.2.1. PE: signs of respiratory distress, tachycardia, use of accessory muscles and cyanosis ... use of accessory muscles of respiration and cyanosis ... 5.3.6.1.1. PE: cyanosis and systemic hypoxemia. 5.3.6.1.2. ECG ...
  • Dyspnea, a low FVC, and/or physical examination findings typical of interstitial fibrosis (rales, clubbing, or cyanosis) raised the risk of subsequent death from asbestos is by 2- to 6-fold. (cdc.gov)
  • Cyanosis may be classified as central or peripheral, referring to the etiology of the hemoglobin desaturation, not to the observed anatomic location of the cyanosis. (medscape.com)
  • Peripheral cyanosis is a manifestation of diminished tissue perfusion with resultant increased local oxygen extraction leading to high levels of desaturated hemoglobin. (medscape.com)
  • Lack of oxygen in the blood causes a bluish discoloration in the skin or mucous membranes called cyanosis. (medlineplus.gov)
  • The distinctive blue or purple skin discoloration of cyanosis indicates the presence of at least 5 g/dL of desaturated hemoglobin. (medscape.com)
  • Most cyanosis is seen as a result of congenital heart disease, pulmonary disease, or as a terminal event as in cardiopulmonary arrest. (medlineplus.gov)
  • Central cyanosis is often a manifestation of congenital heart disease characterized by right-to-left pulmonary shunts. (medscape.com)
  • Cyanotic heart disease is a congenital heart defect which results in low oxygen levels in the blood and causes the child's lips, fingers, and toes to look blue (cyanosis). (mountsinai.org)
  • Cyanosis is a medical condition characterized by blue colored skin and mucous membranes, which occurs as the result of inadequate amounts of oxygenated hemoglobin -- the molecule which carries oxygen to the body tissues -- or due to hemoglobin abnormalities. (petmd.com)
  • It is classified as a cyanotic heart defect because the condition leads to cyanosis, a bluish-purple coloration to the skin, and shortness of breath due to low oxygen levels in the blood. (mountsinai.org)
  • Less oxygen delivered to the body can make the skin look blue ( cyanosis ). (mountsinai.org)
  • Central cyanosis typically involves the entire body but may be best appreciated on warm areas of the body (eg, tongue, oral mucosa, conjunctiva, skin). (medscape.com)
  • Cyanosis refers to a bluish color of the skin and mucous membranes. (mountsinai.org)
  • Depending on what underlying illness is causing the cyanosis, drugs may be prescribed to treat the condition, or surgery and/or further therapy ordered. (petmd.com)
  • Unfortunately, dogs that are suffering from cyanosis caused by advanced lung/airway disease and severe heart disease have a poor long-term prognosis. (petmd.com)
  • After the company switched to a replacement adhesive, Thixon-521, a followup study was performed to check workers for signs of cyanosis or other pertinent adverse health effects. (cdc.gov)
  • A blood chemical profile, complete blood count, urinalysis, electrocardiograph (EKG), thoracic radiographs (and echocardiogram with Doppler, if heart or lung disease is suspected), and an electrolyte panel should be ordered to determine the underlying cause of the disease that is causing cyanosis. (petmd.com)
  • Severely anemic patients (regardless of the degree of desaturation) are, therefore, unable to manifest cyanosis. (medscape.com)
  • Lack of oxygen in the blood causes a bluish discoloration in the skin or mucous membranes called cyanosis. (medlineplus.gov)
  • Cyanosis is a bluish or purplish tinge to the skin and mucous membranes. (medscape.com)
  • Facial cyanosis in a patient with chronic hypoxemia. (medscape.com)
  • Before the era of rapid blood gas analysis, clinicians often assessed hypoxemia on clinical grounds alone, primarily by looking for cyanosis in the perioral area and fingers. (medscape.com)
  • At this level of hypoxemia, the patient would also have other manifestations of hypoxemia (eg, respiratory symptoms, mental status changes) apart from cyanosis. (medscape.com)
  • With a hemoglobin content of less than 9 g/dL, the patient would likely succumb from hypoxemia before cyanosis became evident. (medscape.com)
  • [ 6 ] At the same time, one should not rely on the absence of cyanosis as reassurance that hypoxemia is not present. (medscape.com)
  • For example, central cyanosis can manifest when SaO2 is 79% in a patient with a hemoglobin of 15 g/dL. (medscape.com)
  • A case report of Eisenmenger syndrome (interrupted aortic arch with ventricular septal defect) in a 31-year-old pregnant woman discusses the rare condition of differential cyanosis. (medscape.com)