Cyanosis medical therapy
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mohammed Abdelwahed M.D[2]
Overview
In every neonate presented with cyanosis and shock, congenital heart disease dependent on patency ductus arteriosus should be considered. The physiologic constriction of ductus arteriosus after birth in a neonate whose pulmonary blood flow or aortic blood flow is dependent on PDA leads to shock and collapse in the neonate. Infusion of prostaglan in such a neonate is life-saving and keeps patency ductus arteriosus. Treatment of underlying causes of peripheral cyanosis such as tamponade or cardiogenic shock due to low cardiac output state and peripheral vasoconstriction lead to disappearing of cyanosis.
Medical therapy of Cyanosis
[1]
[2][3][4][5]
Abbreviations:
d-TGA: dextro-Transposition of great arteries;
PDA: Patent ductus arteriosus ;
ASD: Atrial septal defect;
VSD: Ventricular septal defect;
TOF: Tetralogy of fallot;
CHD: Congenital heart disease;
PS: Pulmonary stenosis;
PTE: Pulmonary thromboembolism;
AS: Aortic stenosis;
ARDS: Acute respiratory distress syndrome;
PFO: Patent foramen ovale;
PVR: Pulmonary vascular resistance;
SpO2: Peripheral capillary oxygen saturation.;
FiO2: Fraction of inspired oxygen;
PEEP: Positive end-expiratory pressure;
| Causes of cyanosis | CHD dependent on PDA | CHD with severe restriction of pulmonary blood flow | CHD with severe restriction of systemic blood flow | CHD due to bidirectional shunt | Methemoglobinemia | PTE | Cardiogenic shock | ARDS | Acute mountain sickness | Pulmonary edema | |
|---|---|---|---|---|---|---|---|---|---|---|---|
| Example | Example | Complication of exposue to some drugs such as nitrites and aniline leading to dizziness , coma, chocolate-brown discoloration of blood samples, respiratory distress seizures and myocardial ischemia | Hypoxia due to V/Q mismatch, low cardiac out-put state, acute right ventricular dilation and increased pulmonary vascular resistance | Example |
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Leakage large molecule into alveole leading [[pulmonary edema] | example | Example | |||
| Mechanism of cyanosis | Example | Hypoxia and cyanosis due to constriction of the ductus arteriosus after birth and dependency of the Pulmonary circulation on the patency of the ductus arteriosus | Cyanosis,systemic hypoperfusion, circulatory collapse, metabolic acidosis, shock due to constriction ductus arteriosus and dependency systemic circulation on PDA after birth | Constriction of PDA after birth leading decreased systemic circulation due to mixing of pulmonary and systemic blood flow via PDA |
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Example |
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Central cyanosis due to alveolar hypoxia , pulmonary vasoconstriction, pulmonary hypertension | Example | |
| Treatment | Example | Prostaglandin E1 | Prostaglandin E1 | Prostaglandin E1 |
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Example |
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Respiratory distress syndrome
Surfactant therapy
- Exogenous surfactant replacement therapy is effective in reducing RDS mortality and morbidity in preterm infants.
- It may be natural or synthetic surfactants.
- Natural surfactants have been shown to be more efficient with lower inspired oxygen concentration and ventilator pressures, decreased mortality, and lower rate of RDS complications in preterm infants.
- All patients with RDS, and intubate and administer surfactant to those with persistent severe respiratory distress (defined as requiring a fraction of inspired oxygen [[[FiO2]]] of 0.40 or higher to maintain oxygen saturation above 90 percent or who are apneic.
- If the infant maintains adequate respiratory efforts and has an FiO2 requirement less than 0.30, no additional doses of surfactant are needed.
- Endotracheal intubation has been the standard technique of surfactant administration.
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 pathway causing the tachycardia and should be administered before considering electrical cardioversion. Intravenous amiodarone may also convert atrial fibrillation and 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.
- 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
- 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.
Peripheral cyanosis treatment
Raynaud's phenomenon
- Drug treatment is normally with a calcium channel blocker, frequently nifedipine to prevent artery constriction.
- 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 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 the supervision of a healthcare provider.
Peripheral vascular disease
- 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)
Cilostazol
- Cilostazol is a phosphodiesterase III inhibitor.
- 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
Endovascular Revascularization Modalities
- PTAC
- Stents
- Atherectomy
- Laser
- Cutting balloons
- Thermal angioplasty
References
- ↑ Cucerea, Manuela; Simon, Marta; Moldovan, Elena; Ungureanu, Marcela; Marian, Raluca; Suciu, Laura (2016). "Congenital Heart Disease Requiring Maintenance of Ductus Arteriosus in Critically Ill Newborns Admitted at A Tertiary Neonatal Intensive Care Unit". The Journal of Critical Care Medicine. 2 (4): 185–191. doi:10.1515/jccm-2016-0031. ISSN 2393-1817.
- ↑ Henretig, Fred M.; Gribetz, Bruce; Kearney, Thomas; Lacouture, Peter; Loveiov, Frederick H. (2011). "Interpretation of Color Change in Blood with Varying Degree of Methemoglobinemia". Journal of Toxicology: Clinical Toxicology. 26 (5–6): 293–301. doi:10.1080/15563658809167094. ISSN 0731-3810.
- ↑ Tisi, G M; Wolfe, W G; Fallat, R J; Nadel, J A (1970). "Effects of O2 and CO2 on airway smooth muscle following pulmonary vascular occlusion". Journal of Applied Physiology. 28 (5): 570–573. doi:10.1152/jappl.1970.28.5.570. ISSN 8750-7587.
- ↑ Austin, John H. M. (1973). "Intrapulmonary Airway Narrowing after Pulmonary Thromboembolism in Dogs". Investigative Radiology. 8 (5): 315–321. doi:10.1097/00004424-197309000-00003. ISSN 0020-9996.
- ↑ . doi:10.1164/rccm.201503-0584OC. Check
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