In co-morbid condition, there is occurrence of more than one disease in the same patient. These diseases may be physical, physiological and psychological. These diseases can affect multiple organ systems in the body, however, these diseases may have common or different mechanisms. Obesity hypoventilation syndrome is associated with multiple other conditions like obesity, diabetes, hypertension and psychological disease like depression. Mr. X is also associated with all these conditions. Symptoms of such patients include sleep apnea, increased blood pressure, snoring, excessive daytime sleepiness, drowsiness due to increased CO2 level, headache, chest pain and depression. These should be incorporation of multiple diagnostic tests in such patients which include BMI, estimation of CO2 level, assessment of pain, blood glucose estimation and blood pressure measurement (Chau et al., 2012). In this essay, a case study of Mr.X is discussed, who is associated with the multiple co-morbidities.
Mr. X is a 59-year old man and living with his wife and two sons. He is admitted to the hospital due to sleep apnea, which is mainly associated breathing problem during the sleep. He is also co-morbid with other conditions like obesity, ventilation syndrome, depression and type 2 diabetes. Due to his health conditions he lost his job and as result he developed depression. He is also keeping himself socially isolated because he is ashamed of his weight. In the health assessment, his vital parameters were assessed and it is evident that these parameters were abnormal. His BMI and body weight are 58 m2 and 165 kg respectively. Normal BMI in an adult person should be between 18.5 to 24.9 m2. Normal respiratory rate should be between 12 – 20 bpm in adults, however it is 28 bpm in Mr. X. This condition is called as tachypnea. Normal pulse rate should be between 60 – 100 bpm, however it is 132 bpm in Mr. X. This condition is called as tachycardia. Normal body temperature range should be between 36.1°C to 37.2°C. However, his body temperature is 38.9°C. His systolic blood pressure is 180 and diastolic blood pressure is 90. In this case, there is increase in the systolic blood pressure and normal diastolic blood pressure. Such type of condition is called as isolated blood pressure. In his assessment, it has been observed that his pain score is 7 in the scale of 10. This type of pain is severe pain and with this pain, it is difficult to perform activities of daily living (Timby et al., 2009).
There are multiple pathological mechanisms involved in the obesity. There is mutation in the leptin gene and increase in the leptin expression, which is a satiety factor. Leptin and ghrelin are produced by the adipose tissues and act on the hypothalamus to control appetite. There is increased number and size of adipocytes in the obesity patients like Mr. X. Adipocytes produce various peptides and metabolites which are responsible for the increase in body weight. In type 2 diabetes, there is peripheral insulin resistance and insufficient insulin secretion by pancreatic beta cells. In obsess patients like Mr. X, there is occurrence of insulin resistance, however diabetes develops in patients in whom there is insufficient secretion of insulin to compensate for insulin resistance. In such obese patients, insulin level may be high; however it would be insufficient for the developed high glucose level (Hwang et al., 2012; Reisner, 2013.. Insulin resistance mainly occurs due to increased levels of fatty acids. In case of Mr. X, there might be increased levels of fatty acids due to obesity. These free fatty acids along with proinflamamtory cytokines are responsible for the reduced glucose transport into the muscle cells and elevated levels of glucose production by liver. Hypertension mainly caused due to the dysregulation in the renin–angiotensin–aldosterone system. Renin is responsible for maintaining extracellular volume and arterial vasoconstriction. Renin plays important role in the cleaving angiotensinogen in angiotensin I under the influence of angiotensin converting enzyme. In this cleavage there is production of angiotensin II, which is responsible for the constriction of blood vessels, peripheral resistance and consequently increase in the blood pressure. In the research, it is evident that, obesity is a risk factor for hypertension because of activation of renin–angiotensin in the adipose tissues (Hall et al., 2015; DeMarco et al., 2015).
Depression mainly occurs due to the disturbance in the central nervous system neurotransmitters like serotonin (5-HT), norepinephrine (NE), dopamine (DA), glutamate, and brain-derived neurotrophic factor (BDNF). There is decreased metabolic activity in the neocortical structures and increased metabolic activity in limbic structures. It is evident from the studies that depression can lead to the hypertension in patient like Mr. X. In depressive and hypertensive patients like Mr. X, there is increased sympathetic tone and increased secretion of adrenocorticotropic hormone and cortisol. In depressive patients there is lack of dopamine which may lead to the deficiency of dopamine at key sites in the brain which can leads to development of hypertension. On the other hand hypertension can also leads to depressive state in the individual. Hypertension leads to the cerebrovascular and ischemic changes which may results in the depressive state in the individuals (Rubio-Guerra et al., 2013). In obesity hypoventilation syndrome, there is reduced sensitivity for the increased levels of PaCO2 and leptin resistance. Due to obese condition of the patient, there can be additional mechanical load on the respiratory system, which lead to the respiratory failure. Initially, hypoventilation occurs in daytime and in later stages it leads to the sleep apnea (Mokhlesi, 2010). In the studies, it is evident that there is elevated inflammatory mediators like interleukin-6 (IL-6), tumor necrosis factor alpha (TNF alpha), interleukin-1 (IL-1), interleukin-18 (IL-18), prostaglandin E2 (PGE2) and C-reactive protein (CRP). It is evident that there is direct correlation between BMI and raised plasma levels of IL-6 or TNF alpha. Due to increased inflammation in the peripheral tissues in obesity, there is occurrence of insulin resistance and hypofunctioning of hypothalamic C releasing hormone which lead to the development of sleep apnea (Dabal and BaHammam, 2009).
Most important intervention for Mr. X should be body weight reduction. It is evident that at least 10 kg reduction in the body weight can improve the functioning of the respiratory system. Mr. X is suffering through severe obesity and it is refractory to dietary and therapeutic intervention. In such cases bariatric surgery proved to be more useful. However, care should to be taken while referring Mr. X for bariatric surgery because he is associated with multiple co-morbidities and there may be risk during general anesthesia and post operative complications. There should be incorporation of few mini-invasive and invasive surgical approaches to achieve reduction in body weight. These approaches not only reduce body weight and improve respiratory function but also improve blood pressure and blood sugar levels. Positive airway pressure ventilation (PAP) would be useful in Mr. X because it gives relief from the obstructive component and modify chest wall and lung mechanics in severe obesity patients (Verbraecken and McNicholas, 2013). Oxygen supplementation would be helpful in Mr. X to reverse hypoxemia. However, it should be keep in mind that alone oxygen supplementation would not be helpful in improving sleep apnea in Mr. X. Obese hypoventilation syndrome is usually associated with the co-morbid conditions which mainly affects cardiovascular system, respiratory system and metabolic system. Hence, pharmacotherapy should be provided to Mr. for respective disease condition. Mr. X also should be advised to maintain proper and physical activity. It would be helpful in avoiding further exaggeration of conditions like obesity, hypertension and diabetes (BaHammam, 2015; Shetty and Parthasarathy, 2015).
Individualized discharge planning should be implemented for Mr. X as he is associated with multiple co-morbidities. Discharge planning of Mr. X should comprise of home care, self management, provision of specialized nursing care, formation of groups with similar disease condition for exchange of information, incorporation of social worker for counseling, experts in the community based care, diet modifications, physical exercise, management of depression and anxiety. Accurate information about medications should be provided to the family physician because Mr. X needs to consume multiple medications. Inaccurate administration of single medication may lead to the drug interactions, adverse conditions and multiple complications. Discharge plan should include schedule for follow-up visits and post-discharge support (McMartin, 2013).
Obesity and related co-morbidity like obesity hypoventilation syndrome is a major health condition. As this condition involves multiple disease and systems, there should be incorporation of the multidisciplinary approach for the management of this condition comprising of pharmacological and non-pharmacological management. In such patients, blood pressure, blood glucose and lipid values should be controlled. Management of these conditions would be helpful in avoiding further complications in the patient. Multiple mechanisms are involved in such co-morbid patients and there is requirement of multiple medications for treating each condition. Hence, medications should be administered with care so that these medications should not affect other medical conditions. Also, these medications should not interact with the other medications. This may result in the reducing efficacy of the medication or producing toxicity. In summary, such patients should be managed with incorporation of experts from respective fields and critically analyzing each aspect of the management.
BaHammam, A. S. (2015). Prevalence, clinical characteristics, and predictors of obesity hypoventilation syndrome in a large sample of Saudi patients with obstructive sleep apnea. Saudi Medical Journal, 36(2), pp. 181–189.
Chau, E.H., Lam, D., Wong, J., Mokhlesi, B, and Chung, F. (2012). Obesity hypoventilation syndrome: a review of epidemiology, pathophysiology, and perioperative considerations. Anesthesiology, 117(1), pp. 188-205.
Dabal, L. A., and BaHammam, A. S. (2009). Obesity hypoventilation syndrome. Annals of Thoracic Medicine, 4(2), pp. 41–49.
DeMarco, V. G., Aroor, A. R., and Sowers, J. R. (2014). The pathophysiology of hypertension in patients with obesity. Nature Reviews Endocrinology, 10(6), pp. 364–376.
Hall, J. E., do Carmo, J. M., da Silva, A. A., Wang, Z., and Hall, M. E. (2016). Obesity-Induced Hypertension: Interaction Of Neurohumoral And Renal Mechanisms. Circulation Research, 116(6), pp. 991–1006.
Hwang, L.C., Bai, C.H., Sun, C.A., and Chen, C.J. (2012). Prevalence of metabolically healthy obesity and its impacts on incidences of hypertension, diabetes and the metabolic syndrome in Taiwan. Asia Pacific Journal of Clinical Nutrition, 21(2), 227-33.
McMartin, K. (2013). Discharge Planning in Chronic Conditions. An Evidence-Based Analysis. Ontario Health Technology Assessment Series, 13(4), pp. 1–72.
Mokhlesi, B. (2010). Obesity hypoventilation syndrome: a state-of-the-art review. Respiratory Care, 55(10), pp. 1347-62.
Reisner, H. (2013). Essentials of Rubin's Pathology. Lippincott Williams & Wilkins.
Rubio-Guerra, A. F., Rodriguez-Lopez, L., Vargas-Ayala, G., Huerta-Ramirez, S., Serna, D. C., and Lozano-Nuevo, J. J. (2013). Depression increases the risk for uncontrolled hypertension. Experimental Clinical Cardiology, 18(1), pp. 10–12.
Shetty, S., and Parthasarathy, S. (2015). Obesity Hypoventilation Syndrome. Current Pulmonology Reports, 4(1), pp. 42–55.
Timby, B. K. (2009). Fundamental Nursing Skills and Concepts. Lippincott Williams & Wilkins.
Verbraecken, J., and McNicholas, W. T. (2013). Respiratory mechanics and ventilatory control in overlap syndrome and obesity hypoventilation. Respiratory Care, 14(1), doi: 10.1186/1465-9921-14-132.
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