Caring for Patients with Diabetes - Essay Example

Caring for Patient with Type I Diabetes of the of the Diabetes Mellitus is a chronic disease that requireslong-term medical attention along two lines. It requires constant care to ensure that it does not create any complications and when there are any, it needs to be managed with extreme care. There are 18.2 million diabetes patients in the US and it constitutes over 6.2 % of America’s population according to a study conducted by US health department. The health care cost fro a diabetes patient was $13, 243 against the average citizen’s $2560. It is a disproportionately expensive disease. This paper examines the nursing interventions and holistic care of a patient with type I diabetes. The patient has presented with 30 mmols/ltr of blood sugar and ketones. The patient is drowsy and the pulse rate is counted as 110. The respiration is fast at 25 deep and sighing breaths per minute, acetone on breath and keto-acidosis has been made. Pathophysiology of Type I Diabetes Type I diabetes can occur in patients of any age and is characterised by the inability of the pancreas to secrete the hormone insulin due to autoimmune destruction of the beta cells. It occurs in children quite abruptly, though new antibody tests have been developed to detect new onset adult form of type I diabetes mellitus known as LADA (latent Auto-immune Diabetes of Adults). What distinguishes them from other diabetic patients is the fact that if insulin is withdrawn, they develop ketosis and eventually ketoacidosis. Hence such patients are always dependent on exogenous insulin. Many of the pathophysiological disturbances in a patient with DKA can be measured by a clinician and should be monitored on a real-time basis throughout the course of the treatment. Attention to clinical laboratory data can help the clinician to track and prevent the onset of secondary lethal complications such as hypoglycemia and hyponatremia and hypokalemia. In the absence of insulin, the primary anabolic hormone, muscles and fats as well as the liver do not take up glucose. Counter regulatory hormones such as glucagons, GH and catecholamines enhance triglyceride breakdown into free fatty acids and gluconeogenesis causing an upshot in the level of serum glucose levels in DKA while there is no insulin. Betaoxidation of these free fatty acids then lead to increased ketone body formations. Metabolism in DKA shifts from the normal fed state to the fasting state characterised by fat metabolism. Secondary complications of primary metabolic derangement include an ensuing metabolic acidosis as ketone bodies deplete extra-cellular and cellular acid buffers. The hyperglycaemia induced osmotic diuresis depletes phosphates, potassium, sodium and water together with glucose and ketones. Most commonly, it depletes 10% of body water and 5mEq per kg of body mass of potassium. The total body potassium may be masked by acidosis by sustaining an increased serum potassium level. The levels can fall precipitously once the rehydration and insulin treatments start. Loss of ketoanions in urine with brisk diuresis and intact renal function may also lead to hyperchloremic metabolic acidosis. Frequency In the USA, DKA is seen in patients with type I diabetes. The incidence is grossly 2% patient years of diabetes and almost 3% of diabetes patients initially presenting with DKA. It can occur in type 2 diabetic patients as well though not as a rule. The mortality rate of DKA is nearly 2% per episode. Before the discovery of insulin in 1922, the mortality rate was almost 100 percent. Though patients less than 19 years of age are more prone to DKA, it can occur to a person of any age. History of patients and symptoms at presentation. Clinicians should look out for the classical symptoms of hyperglycemia such as thirst, polyuria, polydispisia and nocturia. Other symptoms include: Generalised weakness Lethargy Nausea Fatigue Decreased perspiration Confusion Increased appetite and Anorexia Clinicians should also be on the look out for associated infections and conditions: Fever Chills Chest Pain Dysuria Shortness of breath Abdominal pain General Signs of patients with DKA Dry skin Ill appearance Dry mucous membranes Decreased skin turgor Decreased reflexes Vital Signs Hypotension Tachycardia Tachypnea Hypothermia Fever (indicative of infection if any) Specific signs Confusion Abdominal tenderness Coma Ketonic breath Causes The most common scenarios are undetected concomitant infection, missed insulin dosages, and newly diagnosed-previously unknown diabetes. Other associated causes make up some 20% of the patients presenting. Urinary infection is the single largest contributor of DKA Myocardial Infarction CVA Complicated Pregnancy Trauma Stress Surgery Idiopathic Also check the patients for Uremia Acute Hypoglycaemic Coma Catheter related Venous Thrombosis particularly for femoral central venous catheters in children Laboratory tests: Blood glucose levels may be as low as 250 mg/dl. A fingerstick glucose test can be administered while waiting for serum chemistry. Hyperglycaemia moves extravascular water to intravascular space. For each 100mg/dl of glucose over the first 100mg/dl, the proportionate fall in sodium is 1.6 mEq/Ltr. When glucose levels tumble, the serum Na will rise correspondingly Potassium needs to be checked regularly as values drop considerably with treatment. An ECG may be administered to check cardiac function. Bicarbonates should be used in conjunction with anion gap to assess the degree of acidosis. Complete blood count. Marked left shift indicate bacterial infection Arterial blood gas levels should be monitored. PH is often sub-7.3 levels Use Acetest and Ketostix products to monitor blood and urine acetone and acetoacetic acid Look for glycosuria and urine ketosis in urinalysis Patients with DKA usually show an osmolality of .330 mOsm/Kg of water. Check for levels of phosphorous especially in patients who had been fasting or on poor diet Hyperamylasemia may be seen BUN is increased Anion gap is higher that usual normal Repeat labs are critical until the patient is normal and should be checked every 1-2 hours. Phosphorous levels should be monitored every four hours or so. Please take care that high serum glucose levels may lead to dilutional hyponatremia; high glyceride levels and subsequent factitious low glucose and high levels of ketone bodies may lead to factitious increase of creatinine. Imaging and Radiological examination A chest radiography should be undertaken to rule out pulmonary infection CT scanning of the brain in children with altered mental status to rule out edema. Administer hypertonic saline or mannitol in those paediatric cases where cerebral edema is suspected. Consider telemetry to observe the patient for ischemia and hypokalemia effects Electrocardiogram: DKA may be precipitated by a cardiac event or the physiological effects of DKA may precipitate a cardiac event Clinical Procedures: Intubation of airway should be done for coma or for cerebral edema. A nastrogastric tube should be administered if the patient is comatose. Isotonic saline should be administered as a bolus up to 1 Litre looking at the patient’s vital signs and other indicators of hypovolemia. Maintain extreme vigilance for any infection, CVA, MI, sepsis or DVT. IV solutions should be administered to combat electrolyte losses and fluid imbalance. Hey also dilute glucose and counter regulatory hormones in the circulatory system. Insulin should be administered to bring back the anabolic metabolism. After initial stabilisation with isotonic saline, switch to half normal saline to combat osmotic diuresis by matching it. Ad 20-40 mlmEg/Ltr equivalent of Potassium Chloride to each litre of fluid administered once K+ counts fall under 5.5mEg/L. K+ can also be administered as two thirds KCL and one third as KPO4. Bicarbonate is typically not replaced although some physicians may resort to it. Phosphae and magnesium toppings are not needed as they stabilise once the patient resumes eating. Typically all patients with DKA are admitted to the hospitals ICU. References: Bell DS, Alele J: Diabetic ketoacidosis: Why early detection and aggressive treatment are crucial. Postgraduate Medicine 1997; 101: 193-8, 203-4[Medline]. Brandenburg MA, Dire DJ: Comparison of arterial and venous blood gas values in the initial emergency department evaluation of patients with diabetic ketoacidosis. Ann Emerg Med 1998; 31(4): 459-65[Medline]. Fearon DM, Steele DW: End-tidal carbon dioxide predicts the presence and severity of acidosis in children with diabetes. Acad Emerg Med 2002 Dec; 9(12): 1373-8[Medline]. Glaser N, Barnett P, McCaslin I: Risk factors for cerebral edema in children with diabetic ketoacidosis. The Pediatric Emergency Medicine Collaborative Research Committee of the American Academy of Pediatrics. N Engl J Med 2001 Jan 25; 344(4): 264-9[Medline]. Green SM, Rothrock SG, Ho JD, et al: Failure of adjunctive bicarbonate to improve outcome in severe pediatric diabetic ketoacidosis. Ann Emerg Med 1998; 31: 41-8[Medline]. Grimberg A, Cerri RW, Satin-Smith M: The "two bag system" for variable intravenous dextrose and fluid administration: benefits in diabetic ketoacidosis management. J Pediatr 1999 Mar; 134(3): 376-8[Medline]. Kitabchi AE, Wall BM: Diabetic ketoacidosis. Med Clin North Am 1995 Jan; 79(1): 9-37[Medline]. Klekamp J, Churchwell KB: Diabetic ketoacidosis in children: initial clinical assessment and treatment. Pediatr Ann 1996 Jul; 25(7): 387-93[Medline]. Ma OJ, Rush MD, Godfrey MM: Arterial blood gas results rarely influence emergency physician management of patients with suspected diabetic ketoacidosis. Acad Emerg Med 2003 Aug; 10(8): 836-41[Medline]. Marinac JS, Mesa L: Using a severity of illness scoring system to assess intensive care unit admissions for diabetic ketoacidosis. Crit Care Med 2000 Jul; 28(7): 2238-41[Medline]. Muir AB, Quisling RG, Yang MC: Cerebral edema in childhood diabetic ketoacidosis: natural history, radiographic findings, and early identification. Diabetes Care 2004 Jul; 27(7): 1541-6[Medline]. Umpierrez GE, Cuervo R, Karabell A: Treatment of diabetic ketoacidosis with subcutaneous insulin aspart. Diabetes Care 2004 Aug; 27(8): 1873-8[Medline]. Warner EA, Greene GS, Buchsbaum MS: Diabetic ketoacidosis associated with cocaine use. Arch Intern Med 1998; 158 (16): 1799-1802[Medline]. Whiteman VE, Homko CJ, Reece EA: Management of hypoglycemia and diabetic ketoacidosis in pregnancy. Obstet Gynecol Clin North Am 1996; 23: 87-107[Medline]. Read More