Cyanosis medical therapy: Difference between revisions
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{{Cyanosis}} | {{Cyanosis}} | ||
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==Overview== | ==Overview== | ||
== | == Initial management of neonantal cyanosis == | ||
* Newborns with cyanosis require adequate tissue perfusion and oxygenation. | |||
* | * An infant who fails the hyperoxia test and does not have persistent pulmonary hypertension of the newborn or a chest radiograph consistent with lung disease is likely to have a cyanotic CHD. | ||
* Monitoring of oxygen level and tissue perfusion is necessary. | |||
* An adequate airway should be established immediately, mechanical ventilation may be needed in case of failed spontaneous respiration. | |||
* Initiating oxygen therapy with 40–60% O2 is sufficient. Exposures to hyperoxia increases oxidative stress and damage lung parenchymal and vascular function. | |||
* In case of a minimal response to oxygen, cardiac disease should be suspected and need for PGE1 should be discussed. | |||
* Cardiac diseases are dependent on a patent ductus to maintain systemic blood flow. | |||
* Oxygen may increase pulmonary blood flow and decrease systemic blood flow. | |||
* Placement of secure intravenous and intraarterial catheters is most easily accomplished via the umbilical vessels. | |||
* Inotropic agents such as dopamine or dobutamine may be necessary to correct '''hypotension'''. | |||
* An isovolumetric partial exchange transfusion should be performed with saline to reduce the hematocrit in cases of severe '''polycythemia'''. | |||
* Maintenance a '''blood glucose''' > 55 mg/dL should be considered. | |||
* '''Acidosis''' should be corrected with infusions of sodium bicarbonate. | |||
* '''Hypocalcemia''' should be corrected based on the ionized calcium. | |||
* Broad spectrum antibiotics should be initiated (ampicillin and gentamicin). | |||
* Closure of the ductus arteriosus can precipitate rapid clinical deterioration with significant life-threatening changes. | |||
* Infants with ductal-dependent lesions are at increased risk for death and significant morbidity unless interventions are initiated to maintain patency of the ductus arteriosus for ductal-dependent lesions, ensure adequate mixing of deoxygenated and oxygenated blood, or relieve obstructed blood flow. | |||
* The initial dose is dependent on the clinical setting, as the risk of apnea, one of the major complications of prostaglandin E1 infusion, is dose dependent | |||
* If the ductus is known to be large in a patient with duct-dependent physiology, the initial dose is 0.01 mcg/kg per minute. This scenario typically is seen in patients with echocardiographic confirmation of a large PDA who are cared for in a tertiary center that provides treatment for neonates with cyanotic heart disease. | |||
* If the ductus is restrictive or the status of the ductus is unknown, the initial dose is 0.05 mcg/kgper minute. This is the standard dose used in patients who require transport to a center with expertise in the care of neonates with cyanotic heart disease. | |||
* The dose of prostaglandin can be increased as needed to a maximum dose of 0.1 mcg/kg per minute. | |||
* Complications of prostaglandin E1 infusion include hypotension, tachycardia, and apnea [8]. As a result, a separate reliable intravenous catheter must be in place to provide fluids for resuscitation. Intubation equipment should be immediately available because apnea can occur at any time during infusion. | |||
== Ebstein's anomaly == | |||
* Control of the heart rhythm with antiarrhythmic drugs: Ebstein's anomaly may present with an [[AV nodal reentrant tachycardia]] with associated [[pre-excitation]]. Among these patients, the preferred pharmacological treatment agent is [[procainamide]]. Since AV-blockade may promote conduction over the [[accessory pathway]], drugs such as [[beta blockers]], [[Calcium channel blocker|calcium channel blockers]] and [[digoxin]] are contraindicated. If there is [[atrial fibrillation]] with pre-excitation, treatment options include [[procainamide]], [[flecainide]], [[propafenone]], [[dofetilide]] and [[ibutilide]] since these medications slow conduction in the [[accessory pathway]]<nowiki/>causing the tachycardia and should be administered before considering electrical [[cardioversion]]. Intravenous [[amiodarone]] may also convert atrial fibrillation and/or slow the ventricular response. | |||
* Inotropic agents and [[diuretics]] for [[heart failure]]. | |||
* Anticoagulation in patients with [[atrial fibrillation]] and [[paradoxical embolization]] Tricuspid valve repair is indicated in patients in which there is symptoms or deteriorating exercise capacity, [[cyanosis]] (oxygen saturation less than 90%), [[paradoxical embolism]], progressive [[cardiomegaly]] on chest x-ray or progressive right ventricular dilation or reduction of right ventricular systolic function. When possible, repair is favored over replacement. [[Warfarin]] is recommended for patients with Ebstein’s anomaly with a history of paradoxical embolus or [[atrial fibrillation]]. | |||
== Coarctation of aorta == | |||
==== Preoperative ==== | |||
* Beta blockers are the treatment of choice. | |||
* Caution should be taken as too much control of hypertension in upper limb can cause hypotension in lower limbs. | |||
* Surgical treatment of the lesion should not be delayed for the correction of hypertension. | |||
==== [[Raynaud's phenomenon | ==== Postoperative ==== | ||
* Immediate post operative hypertension - use short-term vasodilators for e.g. [[sodium nitroprusside]], or intravenous beta-blockers like [[esmolol]]. | |||
* Long-term antihypertensive post surgery | |||
** Monotherapy with [[beta-blockers]] | |||
** [[ACE inhibitors]] or [[angiotensin II antagonists]] may be added if hypertension continues with beta-blocker monotherapy. | |||
== Eisenmenger syndrome == | |||
* If surgical intervention is not available, treatment is mostly [[palliative]] | |||
** Anticoagulants | |||
** Pulmonary vasodilators such as [[bosentan]] | |||
** PGE 5 inhibitor | |||
** Prostacyclin may improve pulmonary artery pressure and may improve length of life | |||
** Antibiotic [[prophylaxis]] to prevent [[endocarditis]] | |||
** [[Bloodletting|Phlebotomy]] to treat [[polycythemia]] | |||
** Maintaining proper fluid balance | |||
** These measures can prolong lifespan and improve quality of life | |||
== Methemoglobinemia == | |||
Methemoglobinemia is treated with supplemental oxygen and [[methylene blue]] 1% solution (10mg/ml) 1-2mg/kg administered intravenously slowly over five minutes followed by IV flush with normal saline. Methylene blue restores the iron in hemoglobin to its normal ([[reduced]]) oxygen-carrying state. This is achieved through the [[Enzyme induction|enzyme inducing]] effect of methylene blue on levels of diaphorase II (NADPH methemoglobin reductase). Diaphorase II normally contributes only a small percentage of the red blood cells reducing capacity but is pharmacologically activated by exogenous cofactors, such as methylene blue, to 5 times its normal level of activity. Genetically induced chronic low-level methemoglobinemia may be treated with oral methylene blue daily. | |||
== Raynaud's phenomenon == | |||
* Drug treatment is normally with a [[calcium channel blocker]], frequently [[nifedipine]] to prevent arterioconstriction. It has the usual side effects of headache, flushing, and ankle [[edema]], and patients often stop treatment, preferring the symptoms of Raynaud's to the symptoms of the drug. | * Drug treatment is normally with a [[calcium channel blocker]], frequently [[nifedipine]] to prevent arterioconstriction. It has the usual side effects of headache, flushing, and ankle [[edema]], and patients often stop treatment, preferring the symptoms of Raynaud's to the symptoms of the drug. | ||
* The extract of the [[Ginkgo biloba]] leaves (Egb 761, 80mg) reduces symptoms in two weeks. | * The extract of the [[Ginkgo biloba]] leaves (Egb 761, 80mg) reduces symptoms in two weeks. | ||
| Line 17: | Line 70: | ||
* Two separate gels combined on the fingertip (somewhat like two-part [[epoxy]], they cannot be combined before use because they will react) increased blood flow in the fingertips by about three times. One gel contained 5% sodium nitrite and the other contained 5% ascorbic acid. The milliliter of combined gel covered an area of ~3 cm². The gel was wiped off after a few seconds. Tucker, A.T. et al., ''The Lancet'', Vol. 354, November 13, 1999, pp.. | * Two separate gels combined on the fingertip (somewhat like two-part [[epoxy]], they cannot be combined before use because they will react) increased blood flow in the fingertips by about three times. One gel contained 5% sodium nitrite and the other contained 5% ascorbic acid. The milliliter of combined gel covered an area of ~3 cm². The gel was wiped off after a few seconds. Tucker, A.T. et al., ''The Lancet'', Vol. 354, November 13, 1999, pp.. | ||
== | == Peripheral vascular disease == | ||
=== Medical Therapy for Acute Occlusion === | === Medical Therapy for Acute Occlusion === | ||
| Line 89: | Line 142: | ||
* Thermal angioplasty | * Thermal angioplasty | ||
* Fibrinolysis/Fibrinectomy | * Fibrinolysis/Fibrinectomy | ||
==References== | ==References== | ||
Revision as of 17:51, 11 March 2018
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:
Overview
Initial management of neonantal cyanosis
- Newborns with cyanosis require adequate tissue perfusion and oxygenation.
- An infant who fails the hyperoxia test and does not have persistent pulmonary hypertension of the newborn or a chest radiograph consistent with lung disease is likely to have a cyanotic CHD.
- Monitoring of oxygen level and tissue perfusion is necessary.
- An adequate airway should be established immediately, mechanical ventilation may be needed in case of failed spontaneous respiration.
- Initiating oxygen therapy with 40–60% O2 is sufficient. Exposures to hyperoxia increases oxidative stress and damage lung parenchymal and vascular function.
- In case of a minimal response to oxygen, cardiac disease should be suspected and need for PGE1 should be discussed.
- Cardiac diseases are dependent on a patent ductus to maintain systemic blood flow.
- Oxygen may increase pulmonary blood flow and decrease systemic blood flow.
- Placement of secure intravenous and intraarterial catheters is most easily accomplished via the umbilical vessels.
- Inotropic agents such as dopamine or dobutamine may be necessary to correct hypotension.
- An isovolumetric partial exchange transfusion should be performed with saline to reduce the hematocrit in cases of severe polycythemia.
- Maintenance a blood glucose > 55 mg/dL should be considered.
- Acidosis should be corrected with infusions of sodium bicarbonate.
- Hypocalcemia should be corrected based on the ionized calcium.
- Broad spectrum antibiotics should be initiated (ampicillin and gentamicin).
- Closure of the ductus arteriosus can precipitate rapid clinical deterioration with significant life-threatening changes.
- Infants with ductal-dependent lesions are at increased risk for death and significant morbidity unless interventions are initiated to maintain patency of the ductus arteriosus for ductal-dependent lesions, ensure adequate mixing of deoxygenated and oxygenated blood, or relieve obstructed blood flow.
- The initial dose is dependent on the clinical setting, as the risk of apnea, one of the major complications of prostaglandin E1 infusion, is dose dependent
- If the ductus is known to be large in a patient with duct-dependent physiology, the initial dose is 0.01 mcg/kg per minute. This scenario typically is seen in patients with echocardiographic confirmation of a large PDA who are cared for in a tertiary center that provides treatment for neonates with cyanotic heart disease.
- If the ductus is restrictive or the status of the ductus is unknown, the initial dose is 0.05 mcg/kgper minute. This is the standard dose used in patients who require transport to a center with expertise in the care of neonates with cyanotic heart disease.
- The dose of prostaglandin can be increased as needed to a maximum dose of 0.1 mcg/kg per minute.
- Complications of prostaglandin E1 infusion include hypotension, tachycardia, and apnea [8]. As a result, a separate reliable intravenous catheter must be in place to provide fluids for resuscitation. Intubation equipment should be immediately available because apnea can occur at any time during infusion.
Ebstein's anomaly
- Control of the heart rhythm with antiarrhythmic drugs: Ebstein's anomaly may present with an AV nodal reentrant tachycardia with associated pre-excitation. Among these patients, the preferred pharmacological treatment agent is procainamide. Since AV-blockade may promote conduction over the accessory pathway, drugs such as beta blockers, calcium channel blockers and digoxin are contraindicated. If there is atrial fibrillation with pre-excitation, treatment options include procainamide, flecainide, propafenone, dofetilide and ibutilide since these medications slow conduction in the accessory pathwaycausing the tachycardia and should be administered before considering electrical cardioversion. Intravenous amiodarone may also convert atrial fibrillation and/or slow the ventricular response.
- Inotropic agents and diuretics for heart failure.
- Anticoagulation in patients with atrial fibrillation and paradoxical embolization Tricuspid valve repair is indicated in patients in which there is symptoms or deteriorating exercise capacity, cyanosis (oxygen saturation less than 90%), paradoxical embolism, progressive cardiomegaly on chest x-ray or progressive right ventricular dilation or reduction of right ventricular systolic function. When possible, repair is favored over replacement. Warfarin is recommended for patients with Ebstein’s anomaly with a history of paradoxical embolus or atrial fibrillation.
Coarctation of aorta
Preoperative
- Beta blockers are the treatment of choice.
- Caution should be taken as too much control of hypertension in upper limb can cause hypotension in lower limbs.
- Surgical treatment of the lesion should not be delayed for the correction of hypertension.
Postoperative
- Immediate post operative hypertension - use short-term vasodilators for e.g. sodium nitroprusside, or intravenous beta-blockers like esmolol.
- Long-term antihypertensive post surgery
- Monotherapy with beta-blockers
- ACE inhibitors or angiotensin II antagonists may be added if hypertension continues with beta-blocker monotherapy.
Eisenmenger syndrome
- If surgical intervention is not available, treatment is mostly palliative
- Anticoagulants
- Pulmonary vasodilators such as bosentan
- PGE 5 inhibitor
- Prostacyclin may improve pulmonary artery pressure and may improve length of life
- Antibiotic prophylaxis to prevent endocarditis
- Phlebotomy to treat polycythemia
- Maintaining proper fluid balance
- These measures can prolong lifespan and improve quality of life
Methemoglobinemia
Methemoglobinemia is treated with supplemental oxygen and methylene blue 1% solution (10mg/ml) 1-2mg/kg administered intravenously slowly over five minutes followed by IV flush with normal saline. Methylene blue restores the iron in hemoglobin to its normal (reduced) oxygen-carrying state. This is achieved through the enzyme inducing effect of methylene blue on levels of diaphorase II (NADPH methemoglobin reductase). Diaphorase II normally contributes only a small percentage of the red blood cells reducing capacity but is pharmacologically activated by exogenous cofactors, such as methylene blue, to 5 times its normal level of activity. Genetically induced chronic low-level methemoglobinemia may be treated with oral methylene blue daily.
Raynaud's phenomenon
- Drug treatment is normally with a calcium channel blocker, frequently nifedipine to prevent arterioconstriction. It has the usual side effects of headache, flushing, and ankle edema, and patients often stop treatment, preferring the symptoms of Raynaud's to the symptoms of the drug.
- The extract of the Ginkgo biloba leaves (Egb 761, 80mg) reduces symptoms in two weeks.
- There is some evidence that Angiotensin II receptor antagonists (often Losartan) reduce frequency and severity of attacks.
- In intractable cases, sympathectomy and infusions of prostaglandins, e.g. prostacyclin, may be tried, with amputation in exceptionally severe cases.
- Alpha-1 adrenergic blockers such as prazosin can be used to control Raynaud's vasospasms under supervision of a health care provider.
- In a study published in the November 8, 2005 issue of Circulation, sildenafil (Viagra) improved both microcirculation and symptoms in patients with secondary Raynaud's phenomenon resistant to vasodilatory therapy. The authors, led by Dr Roland Fries (Gotthard-Schettler-Klinik, Bad Schönborn, Germany), report: "In the present study, capillary blood flow was severely impaired and sometimes hardly detectable in patients with Raynaud's phenomenon. Sildenafil led to a more than 400% increase of flow velocity."
- Two separate gels combined on the fingertip (somewhat like two-part epoxy, they cannot be combined before use because they will react) increased blood flow in the fingertips by about three times. One gel contained 5% sodium nitrite and the other contained 5% ascorbic acid. The milliliter of combined gel covered an area of ~3 cm². The gel was wiped off after a few seconds. Tucker, A.T. et al., The Lancet, Vol. 354, November 13, 1999, pp..
Peripheral vascular disease
Medical Therapy for Acute Occlusion
- Urgent measures should be taken to ensure blood flow and protect the limb:
- ICU admission
- Administration of heparin for anticoagulation
- Electrolytes, acid- base and renal status monitoring
- Limb status monitoring and frequent assessment of the need for fasciotomy.
- If the limb is not immediately threatened:
- Continue treatment with thrombolytic therapy for 14 days.
- If the limb ischemia is critical:
- Consider percutaneous transluminal angioplasty
- Consider surgery: thromboembolectomy, bypass grafting
- Send sample for pathologic examination (myxoma may be present)
Reduction in Modifiable Cardiovascular Risk Factors[edit | edit source]
- Diabetes control
- Hypertension treatment
- Dyslipidemia treatment
- Smoking cessation
Improvement of the Walking Ability[edit | edit source]
Exercise Rehabilitation[edit | edit source]
- A regular walking program four times a week for six month results in an average of 6.5 minutes improvement in the walking time.
- It opens up collateral circulation.
- It reduces cardiovascular mortality.
- It improves quality of life.
Cilostazol[edit | edit source]
- Cilostazol is a phosphodiesterase III inhibitor.
- It is FDA approved.
- Cilostazol is not administered to all PAD cases but rather to selected cases where regular walking program has failed to improve the walking time and capacity.
- It is contraindicated in congestive heart failure.
- Side effects:
- Headache
- Diarrhea
- Gastric upset
- Palpitations
- Dizziness
The Choice of the Revascularization Intervention Based on TASC Classification[edit | edit source]
For detailed information regarding the TASC classification, click here.
Iliac Lesions[edit | edit source]
- Endovascular revascularization is the intervention of choice in patients with TASC type A iliac lesions.
- TASC type A iliac lesions is defined as a single stenosis less than 3 cm of the common iliac artery or external iliac artery (unilateral/bilateral).
- Surgical revascularization is the intervention of choice in patients with TASC type D iliac lesions.
- TASC type D iliac lesions is defined as either one of the following:
- Diffuse, multiple unilateral stenoses involving the common iliac artery, external iliac artery, and common femoral artery (usually more than 10 cm long)
- Unilateral occlusion involving both the common iliac artery and external iliac artery
- Bilateral external iliac artery occlusions
- Diffuse disease involving the aorta and both iliac arteries
- Iliac stenoses in a patient with an abdominal aortic aneurysm or other lesion requiring aortic or iliac surgery.
- TASC type D iliac lesions is defined as either one of the following:
- As for TASC type B iliac lesions and TASC type C iliac lesions, the choice between endovascular and surgical revascularization requires the evaluation of the percentage of artery stenosis.
Femoral Lesions[edit | edit source]
- Endovascular revascularization is the intervention of choice in patients with TASC type A femoropopliteal lesions.
- TASC type A femoropopliteal lesions is defined as a single stenosis less than 3 cm of the superficial femoral artery or popliteal artery.
- Surgical revascularization is the intervention of choice in patients with TASC type D femoropopliteal lesions.
- TASC type D femoropopliteal lesions is defined as complete common femoral artery or superficial femoral artery occlusions or complete popliteal and proximal trifurcation occlusions.
- As for TASC type B femoropopliteal lesions and TASC type C femoropopliteal lesions, the choice between endovascular and surgical revascularization is not definite.
Endovascular Revascularization Modalities[edit | edit source]
- PTAC ( Percutaneous transluminal angioplasty)
- Stents
- Atherectomy
- Laser
- Cutting balloons
- Thermal angioplasty
- Fibrinolysis/Fibrinectomy