We will write a custom Essay on Metabolic Acidosis, Its Diagnosis and Treatment specifically for you
301 certified writers online
A cataleptic African-American male was taken into the emergency unit. The patient was brought directly from a building and construction site. The physician noted that his skin was warm and flushed. He also exhibited a fruity odor breath and tachycardia. As such, his family and friends did not accompany him. Similarly, his records indicated that he had a history of uncontrolled type 1 diabetes mellitus.
Based on the above symptoms and laboratory tests, the patient is suffering from metabolic acidosis (Gordis, 2007). There are numerous forms of metabolic acidosis. They include diabetic acidosis, lactic acidosis, and hyperchloremic acidosis. Because the patient had been diagnosed with diabetes mellitus type 1, he had a higher risk of developing metabolic acidosis. The complication is experienced when the body generates excess acid. Metabolic acidosis can also be exhibited when kidneys fail to get rid of excess acid from the body. The symptoms for the above symptoms include grapey odor, reddened skin, and rapid breathing (Symposium, 2007). Notably, the patient in the case study exhibited the above symptoms.
The patient’s laboratory examination indicated a glucose level of 750mg/dL, a pH level of 7.12, a CO2 rate of 44, and a HCO3 rate at 12. A person with the diabetic acidosis will exhibit a blood glucose level above 250.0mg/dl, a pH level between 7.00 and 7.30, and a HCO3 level of less than 15 (Sirotina, 2005). Notably, the patient in the case study has tested positive for all the above complications (Van & Pijpe, 2005). Thus, the laboratory analysis provided the basis of my identification.
Cause of rapid breathing
In our bodies, sugar is a principal source of energy required by the muscular and tissue muscles (Miller, 2006). Usually, insulin aids the absorption of sugar into the body cells. In the absence of adequate insulin, the patient’s body will not be able to utilize adequate sugar. Under such situations, the body triggers the production of hormones that disintegrate fats to produce energy. The process leads to the generation of ketones. When surplus ketones accumulate in the blood, they are released through the urine. The above complication stabilizes the body pH.
Usually, human bodies are adapted to a constant internal environment and stable pH levels of around 7.4 or above. Lesser pH levels exhibited by the patient in the case study make the body more acidic. Because of this, the human body will attempt to retain stable pH by involving the buffer systems. The buffer systems comprise of chemical constituents, which consume or release H+ that are liable for acidity. CO3– is a significant compound of these buffer systems. It can disintegrate hydrogen ions into very frail H2CO3, which breaks down into H2O and CO2. Carbon dioxide generated through this process accrues in the body. With increased CO2, the patient will experience a hasty breathing. Rapid respirations try to eliminate excess carbon dioxide in the body.
After establishing the level of dehydration from the laboratory analysis, treatment should be initiated. As such, intravenous fluid should be administered to the patient. The patient should be offered with saline of 0.90% at 15.0 to 20.0 mL per kg every hour (Repina, 2007). During the process, the fluids standing, electrolyte rates, and cardiac condition should be monitored. Equally, urine production and blood pressure ought to be evaluated. As the client becomes stable, the fluids should be reduced to between 4 mL to 14 mL per kg every hour or 250.0 to 500.0 mL hourly (Gordis, 2007). When sodium concentration stabilizes, a saline solution of 0.450% should be offered. Dextrose is supplemented once glucose rate drops to 200.0 mg for every dL.
Insulin should be introduced after one or two hours to stabilize the patient’s situation. A preliminary bolus of 0.10 units per kg is given with a mixture of 0.10 units per kg hourly. A mixture of 0.140 units per kg per hour should be used if a bolus is not available. During this process, glucose level is expected to lessen to around 50.0 to 70.0 mg per dL every hour. Therefore, insulin mixture should be attuned to attain this objective.
When the glucose level diminishes to 200.0 mg per dL, insulin mixture ought to be reduced to 0.05 to 0.100 units for every kg every hour. Similarly, dextrose fluids ought to be supplemented with the intravenous solutions at this level to maintain a sugar level ranging from 150.0 mg and 00.0 mg for every dL. The disorder is fixed when the sugar level is below 200.0 mg for every dL, the pH level is higher than 7.3, and when the HCO3 level is 18 mEq per L or more. When the above situations are met, the patient should be initiated on an insulin routine. Because the patient is diabetic, changes should be made on his outpatient prescription to enhance management of the disease. Similarly, the patient should be encouraged to adhere to his medication and diet as instructed by a physician.
Gordis, L. (2007). Using epidemiology to identify the causes of disease Epidemiology. 6(1),215-229.
Miller, W. (2006). Infectious Disease in Epidemiology. Epidemiology, 21(5), 593-594.
Repina, E. (2007). Mechanisms of adaptive immunity exemplified by type 1 diabetes mellitus. DM Journal, 13(2), 51-56.
Sirotina, O. (2005). Thymus in children with type 1 diabetes mellitus. DM Journal, 14(2), 75-76.
Symposium, C. (2007). Metabolic Acidosis. Hoboken: John Wiley & Sons.
Van, G., & Pijpe, A. (2005). E-epidemiology: a comprehensive update. A Epidemiology, 1(1), 172-179.