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Cyanosis is the condition where the skin of a person turns blue or purplish due to reduced oxygen. This bluish color is noticed mostly on the lips, fingers and toes. It is the result of circulatory or heart problems. It is indicative of too little oxygen in the blood. Cyanosistic heart disease is characterised by bluish or grayish skin, tiredness and puffy eyes. Chest pain and fainting might occur.

Causes of cyanosis

Diagnostic tests such as chest x-ray, complete blood count, ECG, Heart MRI, Cardiac catherization and pulse oximeter might be done to ascertain the problem leading to cyanosis. Some congenital heart diseases might need surgery to rectify any birth defect.

Bronchopulmonary Dysplasia

Babies who are born prematurely experience various disorders. These disorders occur because of the underdevelopment of a particular organ. Bronchopulmonary Dysplasia is a very serious condition which occurs predominantly in premature babies. Bronchopulmonary Dysplasia was first noticed in 1976, among pre term babies suffering respiratory distress. The babies were categorized as ventilator dependent as they needed increased oxygen.

Symptoms of Bronchopulmonary Dysplasia

Chronic lung disease or Bronchopulmonary dysplasia occurs because of developmental disorders. The cellular arrangement in the lung tissue is also impaired to a large extent. Babies who are born at a gestation period of 34 weeks are prone to chronic lung disease. Studies imply that babies whose weight is less than 4 pounds during this period also experience symptoms of this condition. This happens because of the reduced development of the alveoli in the lung tissue.

These babies are often treated with positive pressure ventilation (PPV), but since they do not have enough antioxidants, there is a possibility of developing oxygen toxicity. The relation between Bronchopulmonary dysplasia and oxygen toxicity is very significant in understanding the exact cause. In many cases, ventilator associated positive pressure treatment has aggravated the condition. The classical symptoms associated are shortness of breath, cyanosis, increased breathing rate and cough.

Diagnosis of Bronchopulmonary Dysplasia

The treatment options become easier for Bronchopulmonary dysplasia, if the root cause is effectively diagnosed. The major diagnostic parameters that have to be taken in to consideration are:

  • Gestation period of the baby.
  • Underlying intrauterine infections.
  • Duration of ventilator exposure after birth.
  • Estimation of oxygen toxicity during positive pressure ventilation.

Careful analysis has to be done in differentiating respiratory distress condition and bronchopulmonary dysplasia through X-rays as both have significant appearance radiologically. One of the diagnostic identifications includes the oxygen dependency of the patient after initial treatment, as this enables evaluation of the lung functionality in the long term. Other tests that add relevance to the diagnosis include arterial blood gas estimation in case of cyanosis, pulse oxymetry and CT scan.

Treatment of Bronchopulmonary Dysplasia

One of the early ways to treat bronchopulmonary dysplasia was to administer systemic steroids. This method was practiced to minimize ventilator utilization. The only disadvantage was the onset of adrenal suppression; hence the dosage pertaining to these steroids was reduced and was given in combination with hydrocortisone to balance the cortisol levels.

Diuretics are also advised. Inflammation associated with bronchopulmonary dysplasia is treated with inhaled nitric oxide therapy as it facilitates the process of vasodilation. Other treatment options include the administration of vitamin A and E to facilitate free radical removal and enhance immunity. Nutrition is an important factor as it meets the demands of the increased energy levels in these babies and also provides the antioxidants to remove the free radicals formed during metabolic pathways.

Mountain sickness

Mountain sickness or altitude sickness occurs as a result of lower oxygen at higher altitude along with reduced air pressure. It is a series of symptoms such as dizziness, headache, nausea and loss of appetite.

Acute Mountain Sickness (AMS) is a mild form of Altitude sickness which is caused by climbing to greater than 8000 feet (2400 meters above sea level). Hypoxemia - the hypoxia resulting from high altitude, in susceptible individuals can occur owing to poor acclimatization. High Altitude Pulmonary Edema (HAPE) is a serious condition that may affect people prone to Acute mountain sickness. This edema is the accumulation of fluid from pulmonary blood vessels in lungs. This results in shortness of breath, rapid pulse and cough with bloody sputum. If not treated in time, coma and then death might be a possibility.

High Altitude Cerebral Edema (HACE), though rare is the most life threatening form of Altitude sickness where cerebral edema occurs with symptoms other than those of Mountain sickness can include severe headache, loss of coordination, speech abnormalities, altered level of consciousness and seizures. This condition is fatal unless treated in time. Treatment begins with descent to a lower altitude and oxygen therapy. It is suggested to take Dexamethasone to reduce cerebral edema.

Mountain sickness happens with those who have tried to reach faster. If a person suffering from a severe episode of altitude sickness, problems such as shortness of breath, cyanosis, chest constriction and inability to walk might be noticed. It is easier to treat the early signs of mountain sickness. Returning to lower altitude is the safest step. Additional oxygen must be given. Severe symptoms that might arise are pulmonary edema, cerebral edema or retinal hemorrhage. Rest and oxygen usually helps most persons suffering mountain sickness. Aspirin can be taken for headache but sleeping medications must not be taken as they can slow down breathing. A diuretic like Acetazolamide is prescribed. High altitude edema is best treated with Nifedipine.

Tags: #Cyanosis #Bronchopulmonary Dysplasia #Mountain sickness
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Collection of Pages - Last revised Date: May 26, 2024