Pathogenesis Relating to the Clinical Manifestations of Mr. Kirkman
Mr. Kirkman presents with a urinary infection. The urinary tract problem seems to have advanced to the upper urinary tract. With the presented symptoms, the patient was contaminated with bacteria in the lower urinary tract (Gill et al., 2015). The bacteria then colonized the of the urethra and the bladder. An inflammatory response resulted in the lower urinary tract. The inflammatory response led to neutrophil infiltration. Since the problem was not treated at this point, the bacteria multiplied and were able to evade the immune system. Evasion of the immune system was achieved in two ways; the first way, which is true for E. coli, is binding the E. coli to the cells in the lower urinary tract hiding from the immune cells (British Society for Immunology., n.d). Another mechanism is through the formation of biofilm by the bacteria (Hall et al., 2014), which results in the bacteria’s adherence to the surface by the bacteria leading to their survival.
Due to the bacteria’s survival, it ascended to the kidney where the kidney was colonized, resulting in the development of the upper urinary infection. The upper urinary disease is characterized by symptoms such as a burning sensation when urinating, and the pain radiating into the right flank, symptoms already exhibited by Mr. Kirkman. After tent four hours, the condition deteriorated since the bacteria got its way into the blood vessels and the bloodstream. The presence of the bacteria in the blood triggers a systematic inflammatory response, an attempt of the body to contain the bacteria (Kaukonen et al., 2015). The answer is characterized by high temperatures of over 38 degrees Celsius, Heart rate of over 90, symptoms already manifested by Mr. Kirkman.
Once the bacteria are in the bloodstream, white blood cells multiply (as evidenced in the FBC report), significantly trying to contain the bacteria. Due to the increased white blood cells, the blood vessels increase in diameter to aid in the response being initiated by the white blood cells. The increased diameter leads to a decrease in pressure blood pressure, as evidenced by low Mr. Kirkman’s low pressure of 80/42 mmHg. Blood permeability increases due to the actions of the white blood cells. Permeability of blood vessels and fluid buildup makes the circulation of oxygen difficult. Since oxygen circulation in the body is impeded within Mr. Kirkman’s body system, the body resents to making energy for the body through the anaerobic metabolism leading to the buildup of lactic acid within the body (Strong and Walley., 2016). The lactic acid destroys the blood vessels making the coagulating body factors form clots to prevent blood from spilling out from the vessels. Since the process is happening worldwide, the coagulating elements are overstretched, some clots wear off, and blood spills outside the blood vessels. Since the blood is now close to the skin surface, the temperatures recorded are elevated, which is the case with Mr. Kirkman.
The destruction of the blood vessels spreads to the lungs resulting in an acute respiratory distress syndrome (Zheng et al., 2014). Due to this, oxygen absorption in the lungs is impeded; hence, the accessory muscles attempt to elevate the rib cage to accommodate more oxygen. Mr. Kirkman’s use of the accessory muscle is an attempt to restore oxygen deficiency. Due to the injuries inflicted on the kidney, the patient does not excrete the urine as required, hence the catheter’s reason to help drain the urine. The patient’s clinical manifestation is an indication of a sepsis condition, and urgent measures need to be taken to stabilize the patient.
Appropriate Nursing Strategy
The case presented by Mr. Kirkman is urgent, and hence a critical nursing strategy needs to be put in place to contain the sepsis condition from further development. The first thing to do in the process is to start the diagnosis process to ascertain if the problem is experiencing sepsis. The diagnosis could include taking blood samples for cultures to indicate the shock and how severe it is. The important indicators include the lactic acid in the body, which would indicate tissue perforation since the cells no longer receive oxygen (Azuhata et al.,2014). Other tests include ABG to indicate the amount of oxygen in the blood. The last test should be creatinine to ascertain the level to which the kidney has been damaged. Since the cultures and the tests would take long to show the results, Mr. Kirkman would be put in broad-spectrum antibiotics treatment. It is so since the correct disease or the bacteria causing the infection has not been identified at this point.
If the problem persists, Mr. Kirkman can be put under anti-fungal treatment while the correct diagnosis is being awaited. The patient is supplied with IV fluids to restore the pressure. The fluids can be administered using a two-way mechanism to ensure the fluids get into the body quicker. The pressors can also be administered to squeeze down the blood vessels to allow an increase in systematic vascular resistance and hence restore the blood pressure. Lastly, the patient should be monitored to see the progress.
Analysis of the Arterial Blood Gas Results
The buildup of body fluids and an increase in the vessels’ permeability leads to a low supply of oxygen. Since the body needs energy, it resorts to make energy through anaerobic metabolism. The by-product of anaerobic metabolism is lactic acid, which leads to a high build of the same in the body (Maggio., 2018). The buildup of lactic acid in the body makes the pH drop since the body is relatively acidic. The PaO2 normally indicates the oxygen exchange within the body. The oxygen exchange for Mr. Kirkman indicates readings that are lower than the normal ranges. The possible explanation of what the patient could be going through is due to the white blood cells increasing the diameter of the vessels. Once the vessels have increased in diameter, the pressure goes down, the vessels’ permeability increases, and there is an increase of fluid buildup. The activities result in low oxygen circulation within the body and hence the decreased PaO2 levels.
According to (Rawat & Sharma., 2019), PaCO2 levels indicate the extent to which CO2 is being eliminated from the body. The levels for Mr. Kirkman indicates that he is experiencing distress in breathing and hence breathes rapidly. The carbon monoxide levels have gone down since the respiratory system is failing and hence high breathing levels by the patient. The HCO3 levels have gone down due to metabolic acidosis. Since the body carries out the metabolic processes with the low levels of oxygen, the HCO3 levels are increased in the body (Burge., 2018). The bicarbonate levels increase due to CO2 build up hence low levels of HCO3. The BE levels have also gone down because acidosis has set in, and the body is acidic. Lastly, lactate levels have gone significantly high in Mr. Kirkman’s body because the body is carrying out metabolism without oxygen; lactate is produced as a by-product of anaerobic metabolism. So, the lactate builds up in the body since the oxygen supply is low, and the body has to compensate by producing energy for the body without using oxygen.
References
Azuhata, T., Kinoshita, K., Kawano, D., Komatsu, T., Sakurai, A., Chiba, Y., & Tanjho, K. (2014). Time from admission to initiation of surgery for source control is a critical determinant of survival in patients with gastrointestinal perforation with associated septic shock. Critical Care, 18(3), R87.
British Society for Immunology. (n.d). Host − Pathogen interactions and immune evasion. Retrieved from https://www.immunology.org/public-information/bitesized-immunology/pathogens-and-disease/host-%E2%88%92-pathogen-interactions-and
Burge, M. (2018). Physiology, Acidosis, Metabolic. Retrieved from https://www.ncbi.nlm.nih.gov/books/NBK482146/
Gill, K., Horsley, H., Kupelian, A. S., Baio, G., De Iorio, M., Sathiananamoorthy, S., … & Malone-Lee, J. (2015). Urinary ATP as an indicator of infection and inflammation of the urinary tract in patients with lower urinary tract symptoms. BMC urology, 15(1), 7.
Hall, M. R., McGillicuddy, E., & Kaplan, L. J. (2014). Biofilm: basic principles, pathophysiology, and implications for clinicians. Surgical Infections, 15(1), 1-7.
Kaukonen, K. M., Bailey, M., Pilcher, D., Cooper, D. J., & Bellomo, R. (2015). Systemic inflammatory response syndrome criteria in defining severe sepsis. New England Journal of Medicine, 372(17), 1629-1638.
Maggio, P. (2018). Sepsis and Septic Shock. Retrieved from https://www.msdmanuals.com/professional/critical-care-medicine/sepsis-and-septic-shock/sepsis-and-septic-shock
Rawat, D., & Sharma, S. (2019). Hypercapnea. Retrieved from https://www.ncbi.nlm.nih.gov/books/NBK500012/
Suetrong, B., & Walley, K. R. (2016). Lactic acidosis in sepsis: it’s not all anaerobic: implications for diagnosis and management. Chest, 149(1), 252-261.
Zheng, G., Huang, L., Tong, H., Shu, Q., Hu, Y., Ge, M., … & Xu, J. (2014). Treatment of acute respiratory distress syndrome with allogeneic adipose-derived mesenchymal stem cells: a randomized, placebo-controlled pilot study. Respiratory research, 15(1), 39.