Hyperosomar Hyperglycaemia Syndrome - Case Study Example

? Hyperosomar Hyperglycaemia Syndrome Introduction Hyperosomar Hyperglycaemia Syndrome is a condition in which a patient’s blood-glucose level is very high, but ketones are not present in the patient’s urine or blood (The Healthy Living Magazine, 2013). This essay investigates Mrs. L and provides the clinical manifestations and patient management and interventions that were applied while taking care of her in the Emergency Department. Mrs. L, a fifty-year old female was brought to the Hospital’s Emergency Department in an ambulance, after she had fallen down while in her bathroom. She was accompanied by her daughter. Mrs. L had a three-day history of confusion, lethargy and drowsiness. She complained of thirst for the last one week, drinking more than eight pints of water a day. Upon registration at the ambulance registration desk of the Emergency Department by administrators, Mrs. L was placed in a separate room, within the department for exceptional care. She was intubated and ventilated because of hypoxemia and poor conscious level, after which her fracture was attended to. Examination showed that the patient had a heart rate of 130, body temperature of 38.2 degrees Celsius, blood pressure of 150/80 and fair chest excursion, with loose wheezes, and serum pH of 7.5. Mrs. L was also dehydrated, as evidenced by her dry mucous membranes. Mrs. L’s spO2 reading was 80%. A blood sample was taken for checking. After the Doctor’s check ups, Mrs. L’s blood glucose was diagnosed with excess of 56. 5mmol. Therefore, her blood glucose was elevated. Tests involving Mrs. L’s urine were positive for glucose; however, she took long to pass urine. She was transferred to the resuscitation room to receive specialised care because she was categorised as having life-threatening conditions and injuries. After investigation from her close family member, the accompanying daughter, it was revealed that Mrs. L had fallen while she at the bathroom. That is why she had a fracture femur. Her family history was also significant for diabetes and hypertension. Clinical Manifestations Dehydration Dehydration is the insufficiency in the amount of water in the human body. It is prudent to identify and treat dehydration early enough to prevent further complications (Konrad, Corrigan, Hamilton, Steiger, & Kirby, 2013). This is because mild dehydration is known to cause tension and fatigue (Ganio & Armstrong, 2011). It can also cause lack of focus, according to (Szalavitz), 2012. It was established from clinical tests that Mrs. L had dry lips and was dizzy, as well as, confused. Mrs. L also had dry mucous membranes. This was enough evidence that the patient was dehydrated. Most of the patients who are dehydrated are normally confused, dizzy, with dry lips and mucous membranes (Campbell, 2011) and (Heit, 2013). It was found out that the patient had complained of thirst for the previous one week, drinking more than eight pints of water a day, from the history of Mrs. L, provided by her daughter. It is healthy to drink lots of water but excessive thirst, and the frequent urge to drink too much water, exhibited by Mrs. L was a sign of dehydration. Finally, the fact that it took long for the patient to pass urine that was required for urine tests was a sign of dehydration. Hyperosomar Hyperglycaemia Syndrome is characterised by hyperglycaemia, extreme dehydration and hyperosmolar plasma (Balasubramaniyam, Palanis, & Rajamani, 2011). Hyperosomar Hyperglycaemia Syndrome is characterised by severe hyperglycaemia. This is a marked increase in serum osmolality and clinical evidence of dehydration, without the accumulation of acetoacetic ketoacids (Venkatraman & Singhi, 2006). Hyperglycaemia results from either an absolute or relative insulin deficiency. It ca also be a result of decreased tissue responsiveness to insulin, which is an increased insulin resistance. This results into gluconeogenesis and glycogenolysis, leading into a reduced rate of glucose uptake and utilization by peripheral tissues. A rise in blood-glucose level follows, leading to dehydration. Hyperosomar Hyperglycaemia Syndrome comes on over several days, and as a result; it is associated with extreme dehydration and metabolic imbalances (Joint British Diabetes Societies, 2012). Most patients with diabetes have blood sugar levels that exceed 600mg/dL (Upstate Medical University, 2008). These sugar levels are extremely higher than the normal blood sugar. Normally, kidneys try to eliminate the extra sugar by putting through urine. Therefore, kidneys put more sugar into urine, and one is made to urinate frequently. Consequently, a lot of body water is lost through excessive urination. Dehydration results due to loss of body fluids. When the body becomes more dehydrated, blood becomes thicker and more concentrated with sugar. This condition deteriorates because the blood becomes more concentrated with sugar due to continued dehydration. The blood sugar concentration reaches a point where it is too high for the kidneys to correct. Therefore, a person is unable to drink enough water that can help rectify the severe problem. Consequently, high blood sugar and dehydration create an imbalance of minerals such as potassium and sodium (Upstate Medical University, 2008). Furthermore, when there is a rise in osmolality in the extracellular fluid, a shift of water from intracellular to the extracellular space results, leading to intracellular dehydration (Venkatraman & Singhi, 2006). Physical findings of HHS have shown intense dehydration among patients, which results from poor tissue turgor. It should be noted that severe dehydration may lead to seizures, and even death (American Diabetes Association, 2013). Confusion, Lethargy and Drowsiness Confusion, drowsiness and lethargy are some of the common symptoms exhibited by patients who are likely to have Hyperosomar Hyperglycaemia Syndrome. Confusion refers to the laxity in thinking at a normal pace. From history of the patient, provided by her daughter, it was established that Mrs. L showed signs of confusion before she hospitalised. The daughter said that her mother could not provide rights answers when she was asked about date and other simple questions. The daughter also alleged that Mrs. L claimed that she like sleeping during most of the day’s time. She complained of being weak, and this was evidenced by her failure to perform simple tasks that she could perform; days before her health condition changed. Hypoglycaemia may lead to alteration of one’s mental function, which may lead to confusion, lethargy and impaired concentration, in turn (Tomky, 2013). Furthermore, confusion may be a result of lack of sufficient glucose to the brain, which impairs its functioning or shuts it down. Deficiency in insulin and peripheral insulin resistance leads to hyperglycaemia, electrolyte imbalance and dehydration. As dehydration persists, it leads to further imbalance in electrolyte levels. Consequently, high blood sugar and dehydration create an imbalance of minerals such as potassium and sodium, which leads to mineral depletion in the skeletal muscles. This leads to lethargy and drowsiness. The brain requires energy in the form of glucose in order to function properly. Unlike other body organs, the brain stores an extremely small amount of energy, compared with its high rate of glucose utilization (Benton, Parker, & Donohoe, 2008). According to the by Yale school of medicine, the brain requires fructose and glucose for proper functioning (Yale University, 2013). Therefore, the brain relies on a continuous glucose supply. The source of glucose is vital for the brain’s physiological functioning. Tight regulation of glucose metabolism is critical for brain physiology (Mergenthaler, Lindauer, Dienel, & Meisel, 2013). When there is insufficient supply of glucose to the brain, its functioning is hampered. This leads to confusion, lethargy and drowsiness, as the brain shuts down. Neurologic impairment is related to the effective serum osmolality (Stoner, 2005). Fever/ High Body Temperature Hyperosomar Hyperglycaemia Syndrome is characterised by elevated body temperature. The body temperature of a healthy person is 37 degrees Celsius. Therefore, when body temperature is high and above this normal level, the patient is characterised with fever. Examination showed that Mrs. L’s body temperature was 38.2 degrees Celsius, which was high enough to rank as the symptom of Hyperosomar Hyperglycaemia Syndrome. It is thought that elevated body temperatures and Hyperosomar Hyperglycaemia Syndrome may be related, though these potentially deleterious interaction remains of high body temperature remain to be explained (Gordon, Katz, & Leon, 2012). Hyperosomar Hyperglycaemia Syndrome is characterised by dehydration. The loss of body fluids among diabetics is what leads to dehydration. As the body becomes more dehydrated, one’s blood becomes thicker and more concentrated with sugar. This condition may deteriorate further, as blood can become more concentrated with sugar, as further dehydration continues. Consequently, the kidneys fail to correct blood sugar concentration because it almost reaches the saturation point. This results into an imbalance of minerals such as potassium and sodium. Subsequently, there is poor skin blood flow, compromised thermoregulation, which leads to high body temperatures. People with Hyperosomar Hyperglycaemia Syndrome have poor circulation to the skin (Scholarly Editions, 2012). Hypoxia After clinical assessment, there was clinical evidence of hypoxia. Besides, the use of the pulse oximeter to read the spO2 and the reading was 80% on room air for Mrs. L, which was less than the recommended 95% or more on room air. A nonrebreather mask was used to administer high concentration of oxygen. Hyperosomar Hyperglycaemia Syndrome is characterised with a reduction in the colloid osmotic pressure that results in lung water content and decreased lung compliance (Kitabchi, Umpierrez, Murphy, & Kreisberg, 2012). Insulin resistance in the body leads to an increased nerve arteriovenus flow and reducing the nutritive flow of normal nerves. In this case, the hypoxic tissues with normal energy substrates fair poorly because there is inefficient anaerobic metabolism. Furthermore, in diabetes, there is an increase in whole blood or plasma viscosity and reduced red blood cell deformability results in a reduction of blood flow, and consequently, hypoxia (Joslin & Kahn, 2005 and Effros, 2012). Patient Management and Interventions Triage Mrs. L was separated from other patients and put in a separate room because she required prioritized care because of the severity of her condition. Her fracture and unconscious condition dictated that she was to be assigned a higher degree of urgency in health care. This patient management intervention required that Mrs. L’s problem was to be identified; alternatives be determined and the most appropriate, among these alternatives was to be chosen. To determine and identify Mrs. L’s problem, information was gathered from her close family member, the daughter who had accompanied her to the hospital. She provided information pertaining to Mrs. L’s pre-hospital health condition. The history provided by the daughter was crucial in establishing that Mrs. L Mrs. L had shown signs of confusion for three days, and that she had symptoms of lethargy and drowsiness. It was also found out that Mrs. L had complained of thirst for one week prior to hospitalisation, as she drank more than eight pints of water a day. A-G Assessment A-G assessment was carried out because Mrs. L’s condition required diagnosis and administration of her severe, primary health problem, given that she was aging. This assessment also provided aid in assessing Mrs. L’s physical assessment and in clinical decision-making. Through this A-G assessment, it was possible to carry out a comprehensive assessment of Mrs. L clinical conditions, especially on her nonverbal, cognitively impaired or functionally impaired clinical conditions. It was also possible to carry out an assessment of physiological and functional changes that might have occurred on Mrs. L because of her aging. Therefore, her age-related risk factors were assessed. It was through the A-G assessment that analysis of manifestation of health disorders such as dehydration was done on Mrs. L. Mrs. L’s oxygen saturation on room air was below the normal range. This was an implication of low cellular perfusion of oxygen in blood, which might have been the cause of insufficient supply of oxygen to the brain, resulting to confusion and drowsiness. Mrs. L exhibited symptoms such as dry lips, dry mucous membranes, which is a common phenomenon for patients who are hyperkalaemic, caused by the hyperglycaemia. This might have been a result of the increased osmotic pressure, which caused potassium loss from cells into the blood stream and sodium into the cells, and was followed by dieresis, leading to dehydration. A-G assessment model was used for Mrs. L because she was older, and from past experience, most of the middle to old age patients who exhibit the aforesaid symptoms may be having undiagnosed diabetes, and they could be in risk of other illnesses. Airway Management and Maintenance of Adequate Ventilation Mrs. L was endotracheal intubated, shortly after arrival at the department because of her status at arrival. A patient who is in comma or whose mental status appears altered requires an establishment of an airway by manual manoeuvre. Therefore, mechanical ventilation was instituted for Mrs. L because she exhibited signs of respiratory failure. After her condition improved, Mrs. L was allowed to maintain own airway, though her respiratory rate was still lower than the normal rate. Mrs. L’s room was also put under positive-pressure ventilation because of her inadequate respiratory rate, until her condition improved. Fluid Management Fluid Management was carried out on Mrs. L to determine her rehydration requirements and prevent deterioration of her health condition. Fluid management helped protect Mrs. L from risks such as Hypovolaemic shock, which is common among old patients. Hypovolaemic shock is a medical condition that occurs when there is a rapid fluid loss due to inadequate perfusion (Ciammaichella, 2013). Hypovolaemic shock occurs when there is inadequate circulating plasma volume in the body. This leads to inadequate tissue perfusion due to decreased blood flow, oxygen delivery and glucose supply to fundamental organs of the body such as the brain (Ames & Federle, 2009). To prevent an altered fluid balance, there was frequent measuring of Mrs. L’s fluid balance to ensure optimal hydration. This helped to prevent severe dehydration, which was likely to cause hypovolaemic shock, and even organ failure, in turn. Urine output, which was observed, was essential in fluid management for the patient because it was used as an observation of Mrs. L to make any early-warning sign score. It is crucial in facilitating rehydration. A goal cannula was inserted in Mrs. L’s fore arm, by the doctor, to test for normal saline on intravenous fluids. Furthermore, human soluble insulin infusion was done. It was through these procedures that observations were made, and recommendation was made for an aggressive treatment with intravenous fluids. The patient took long to pass urine, but she was reviewed frequently. Compensated metabolic acidosis was detected through the results of the tests carried. Later, when a goal cannula was inserted in Mrs. L’s other arm, it was discovered that the rate of insulin infusion had changed. The insulin infusion was carried out to achieve a steady glucose decline in plasma glucose. Monitoring of capillary blood glucose was done frequently to determine the right insulin dosing for Mrs. L until she could achieve a stable glucose level. Concentrated urine was drained from the patient to aid in monitoring of fluid output. On testing, the urine for ketones, negative results were obtained. Fluid management played an extremely significant role in assessing Mrs. L’s health condition. The administering of normal saline and the continuous reassessment to ascertain and determine Mrs. L’s response to fluid administration was crucial because it helped in looking for evidence of over-hydration. This also involved the assessment of blood glucose, which is also essential (Mistovich, 2008). Pharmacological Interventions Insulin Replacement Mrs. L’s insulin levels were restored with an initial IV bolus of intravenous insulin. This was followed by continuous infusion at a rate of 0.1 Units/Kg/Hr. Later, when Mrs. L’s blood glucose had gone down to the normal level, infusion was reduced to 0.05 Units/Kg/Hr. Then, a normal saline dextrose fluid was infused at a rate of 150 mL/hr. The insulin dosage was then adjusted frequently to maintain blood-glucose levels of 200 mg/dL. Intravenous insulin was used to avoid making errors in restoring the blood sugar of the patient. This is because insulin levels cannot be lowered quickly, in response to excessive dosing, and avoiding hyperglycemia may be difficulty, but intravenous dosing gets rid of these problems (Lehne, 2013). Rehydration, Sodium and Potassium Replacement Since the patient was dehydrated, there had to be rehydration and replacement of sodium that was lost. This condition was corrected using IV saline at 0.9%. 8 L of the IV saline fluid was used for the first eleven hours that Mrs. K received treatment. Potassium phosphate was used to replace potassium loss at a rate of 0.2 mEq/ Kg/Hr. Potassium replacement for Mrs. L started shortly after she was admitted. Conclusion Hyperosomar Hyperglycaemia Syndrome is a condition of severe hyperglycemia and dehydration, and if it develops in poorly controlled diabetes, it can lead to electrolyte loss. Hyperosomar Hyperglycaemia Syndrome is also known to cause death, according to (Joseph, Jerrams, Sivapackianathan, & Chowdhury), 2012. Additionally, there is an increased risk of Hyperglycaemia and high blood pressure, which are associated with death (Khan, Vasudevan, Arjomand, Ali, & Shahzad, 2011). Therefore, it is imperative to manage patients in critical condition, in critical care settings. Serum glucose and body temperatures should be observed, but their management remains controversial (Lukovits & Goddeau, 2011). The investigation, clinical manifestations, patient management and pharmacological interventions that were applied to Mrs. L, a patient who was attended to, at the Emergency Department shows that diabetes, if undiagnosed can lead to fatal consequences. For instance, her condition had led to a fracture femur, after she fell. She was intubated and ventilated because of hypoxemia and poor conscious level. Furthermore, examination results revealed the Mrs. L had a high rate of heart beat, high body temperature. The patient was also dehydrated. After the examination of her blood sample, Mrs L’s blood glucose was diagnosed with excess of 56. 5mmol, meaning it was elevated. Also, tests carried on Mrs. L’s urine were positive for glucose. Among the symptoms that were used to diagnose Mrs. L’s condition were dehydration, confusion, lethargy and drowsiness. Dehydration of the patient may have resulted from high glucose levels in the blood. In the bid to reduce this high level of glucose in blood, the kidneys allocated more sugar in urine, increasing the urge of the patient to urinate frequently. Consequently, this led to fluid and electrolyte loss. Poor blood circulation, might have also led to confusion because the functioning of the brain might have been hampered. This might have also been the cause of the high body temperature that the patient exhibited. The patient management interventions applied in providing care for Mrs. L include triage, A-G assessment, fluid management and airway management and maintenance of adequate ventilation. Triage facilitated the separation of Mr. L to enhance prioritised and specialised care because she was in a critical condition, while A-G assessment was crucial in the diagnosis and administration of her severe, primary health problem, given that she was older. Airway management and maintenance of adequate ventilation ensured that the patient’s respiration could be sustained, while fluid management could help in the management of the patient’s condition. Hyperglycaemia is common during critical illnesses (Cely, Arora, & Quartin, 2005). Therefore, appropriate health care was necessary to prevent further complications. Insulin replacement, rehydration, sodium and potassium replacement was among the pharmacological interventions that were applied in the treatment of Mrs. L. Insulin replacement helped in the management of plasma glucose to facilitate normal functioning of the body. This helped in rehydrating the patient. Sodium and potassium replacement was vital in the maintenance of electrolyte level, which would ensure normal metabolic processes. It would also maintain the ion-water balance in the body. Body temperature could also be regulated appropriately, when metabolic reactions were normalised, and there was a balance in electrolyte level. The main objective of this individualised health care was to rehydrate the patient, while maintaining electrolyte homeostasis, and to correct hyperglycemia. Such treatment should also involve the treatment of underlying diseases and monitoring of the respiratory and the central nervous system functioning (Hemphill & Schraga, 2013). References American Diabetes Association. (2013, August 21). Hyperosmolar Hyperglycemic Nonketotic Syndrome. Retrieved from http://www.diabetes.org/living-with-diabetes/complications/hyperosmolar-hyperglycemic.html Ames, J. T., & Federle, M. P. (2009). CT Hypotension Complex (Shock Bowel) Is Not Always Due to Traumatic Hypovolemic Shock. American Journal of Roentgenology , 1-7. Balasubramaniyam, N., Palanis, C., & Rajamani, ,. V. (2011). Hyperosmolar Hyperglycemic Nonketotic Syndrome Presenting With Hemichorea-Hemiballismus: A Case Report. Journal of Neuropsychiatry & Clinical Neurosciences , 1-5. Benton, D., Parker, P. Y., & Donohoe, R. T. (2008). The Supply of Glucose to the Brain and Cognitive Functioning. Journal of Biosocial Science , 463-479. Campbell, N. (2011). Dehydration: Why is it Still a Problem? Nursing Times Journal , 12-15. Cely, C. M., Arora, P., & Quartin, A. A. (2005). Relationship of Baseline Glucose Homeostasis to Hyperglycemia During Medical Critical Illness. CHEST Journal , 1-8. Ciammaichella, M. M. (2013). Hypovolemic Shock. EM Journal , 1-10. Effros, R. (2012). Microcirculation: Current Physiologic, Medical and Surgical Concepts. Oxford: Elsevier Science Press. Ganio, M. S., & Armstrong, L. E. (2011). Mild Dehydration impairs Cognitive Performance and Mood of Men. British Journal of Nutrition , 1535-1543. Gordon, C. J., Katz, L., & Leon, L. R. (2012). Mechanisms of Hypothermia, Delayed Hyperthermia and Fever Following CNS Injury. American Journal of Neuroprotection and Neuroregeneration , 4-19. Heit, J. (2013). Dehydration. ALBUQUERQUE Journal , 1-4. Hemphill, R. R., & Schraga, E. D. (2013). Hyperosmolar Hyperglycemic State Treatment & Management. Retrieved from http://emedicine.medscape.com/article/1914705-treatment Joint British Diabetes Societies. (2012, August). The Management of the Hyperosmolar Hyperglycaemic State (HHS) in Adults with Diabetes. Retrieved from http://www.diabetologists-abcd.org.uk/JBDS/JBDS_IP_HHS_Adults.pdf Joseph, A., Jerrams, S., Sivapackianathan, R., & Chowdhury, T. A. (2012). Fatal Hyperosmolar Hyperglycaemic Syndrome Complicated by Rhabdomyolysis. Journal of the Royal Society of Medicine , 1-3. Joslin, E. P., & Kahn, C. R. (2005). Joslin's Diabetes Mellitus. Philadelphia: : Lippincott Williams & Willkins Press. Khan, I., Vasudevan, V., Arjomand, F., Ali, R., & Shahzad, S. (2011). Quetiapine Induced Fatal Neuroleptic Malignant Syndrome( NMS) and Hyperosmolar Hyperglycemic Nonketotic Coma (HHNC). CHEST Journal , 1-2. Kitabchi, A. E., Umpierrez, G. E., Murphy, M. B., & Kreisberg, R. A. (2012). Hyperglycemic Crises in Adult Patients With Diabetes. Diabetes Journal , 1-10. Konrad, D., Corrigan, M. L., Hamilton, C., Steiger, E., & Kirby, D. F. (2013). Identification and Early Treatment of Dehydration in Home Parenteral Nutrition and Home Intravenous Fluid Patients Prevents Hospital Admissions. SAGE Journal , 1-8. Lehne, R. A. (2013). Pharmacology for Nursing Care. St. Louis: Elsevier Press. Lukovits, T. G., & Goddeau, R. P. (2011). Critical Care of Patients With Acute Ischemic and Hemorrhagic Stroke. CHEST Journal , 1-3. Mergenthaler, P., Lindauer, U., Dienel, G. A., & Meisel, A. (2013). Sugar for the Brain: the Role of Glucose in Physiological and Pathological Brain Function. The American Journal of Medicine , 587-597. Mistovich, J. (2008, March 24). Understanding the Presentation of Hyperglycemic Hyperosmolar Nonketotic Syndrome . Retrieved from http://www.ems1.com/ems-products/consulting-management-and-legal-services/articles/392581-Understanding-the-Presentation-of-Hyperglycemic-Hyperosmolar-Nonketotic-Syndrome/ Scholarly Editions. (2012). Advances in Rehabilitation Research and Application: 2012 Edition. Georgia: Scholarly Editions Press. Stoner, G. D. (2005). Hyperosmolar Hyperglycemic State. Journal of the American Physician , 1723-1730. Szalavitz, M. (2012). Bad Mood, Low Energy? There Might Be a Simple Explanation. Journal of Nutrition , 1-10. The Healthy Living Magazine. (2013). Hyperosmolar Hyperglycemic Syndrome. Retrieved from cast.diabetes.org/diabetes-101/hyperosmolar-hyperglycemic-syndrome Tomky, D. (2013). Detection, Prevention, and Treatment of Hypoglycemia in the Hospital . Diabetes Journal , 1-12. Upstate Medical University. (2008). Hyperosmolar Hyperglycemic State. Retrieved from http://library.upstate.edu/articles/patients/eil/endo3913.php Venkatraman, R., & Singhi, S. C. (2006). Hyperglycemic Hyperosmolar Nonketotic Syndrome. Indian Journal of Pediatrics , 55-60. Yale University. (2013). Fructose on Brain may Promote Overeating. The Journal of the American Medical Association , 1-10. Read More