YS is a fourteen-year-old Korean girl who was previously hospitalized for contracting measles following an outbreak in her state of residence. Apparently, her family had been reluctant to get her immunized against measles as they had preoccupations about the relationship between the MMR (measles, mumps, and rubella) vaccine and autism. She, however, has no history of major traumas or surgeries. YS is currently suffering from type 1 diabetes mellitus. Additionally, there is a history of DM on her paternal side of the family. The patient was admitted to the hospital following a primary diagnosis of diabetic ketoacidosis. The patient started feeling tired and nauseated in the morning. She, however, insisted on going to school as she had to rehearse for her upcoming dance performance. In the course of her rehearsal, she became fatigued and began throwing up while complaining of abdominal pains. She visited the school’s sanatorium where the nurse in charge picked out a fruity smell from her breath. Additionally, she presented with polyuria and hyperglycemia as her blood glucose level is 359 mg/dL. Her blood pressure is, however, within the range of normalcy for her age and sex as it stands at 100/68 mmHg.
Normal Glycemic Control
Four key players are involved in the regulation of blood glucose. Two of them are organs – the liver and the pancreas, while the other two are hormones – insulin and glucagon. The alpha and the beta cells located in the pancreatic Islets of Langerhans secrete glucagon and insulin respectively. Glucose is the primary source of energy for the body, and as such, it is tightly controlled. Insulin facilitates the uptake and utilization of glucose by cells. It binds to specific insulin receptors on the cell membrane which then undergoes conformational changes to permit the influx of glucose. As such, insulin assists the body in glycemic control. On the other hand, glucagon, a powerful hyperglycemic stimulant, acts on the liver to stimulate the production of glucose (Giugliano, Ceriello, & Esposito, 2008) through glycogenolysis and gluconeogenesis.
Definition of Pathologies
Diabetes mellitus (DM) is a chronic metabolic disorder that is acquired or inherited and is characterized by an elevation of the sugar levels in the blood for a protracted period. As such it manifests as polyuria, polydipsia, and polyphagia. It affects the ability of the body to utilize glucose (Mayo Clinic Staff, 2014b) by interfering with the production and functionality of insulin. Prolonged hyperglycemia leads to long-term dysfunction, failure and damage to organs including the heart, nerves, kidneys, blood vessels, and eyes. There are four main types of DM. Type 1 is insulin-dependent as opposed to type 2 which manifests due to insulin resistance. Type 3 is drug-induced, and type 4 is gestational.
Type 1 DM, also referred to as juvenile diabetes or insulin-dependent DM (IDDM), is further divided into two: a and b. Type 1a is an autoimmune disorder in which cells from the body’s immune system attack the beta cells of the pancreas thus inhibiting the production of glucose. Type 1b is idiopathic. Type 1 DM develops at any age but is common in patients below the age of forty (Diabetes UK, 2017). Diabetic ketoacidosis (DKA) is a life-threatening complication that occurs in patients with diabetes when their insulin levels get to very low concentrations. As a consequence, the amounts of ketones build up in the body. DKA is commonly a complication of type 1 DM but occasionally manifests in type 2 diabetes patients.
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DKA stems from the relative or absolute shortage of insulin that triggers the elevation of an upsurge of cortisol, epinephrine, growth hormone, and glucagon which are counter-regulatory hormones. Due to the body’s inability to mobilize glucose for energy, it resorts to employing alternative fuels. The hepatocytes initiate lipolysis, glycogenolysis, and gluconeogenesis. Increased lipase activity leads to producing free fatty acids metabolized to acetyl-CoA which enters the Citric Acid cycle to produce energy; the other bit is converted to ketone bodies which mount up rapidly in the body resulting in ketonemia. Catabolism of proteins and glycogen yields glucose leading to hyperglycemia. When these metabolites exceed the body’s elimination capacity, the kidneys eliminate the excess glucose and ketone in the urine causing glucosuria and ketonuria. Progressively, the accumulation of these acidic metabolites causes ketoacidosis typified by a marked decrease in bicarbonate and pH (Hamdy, 2017). Acidosis and hyperosmolarity, dehydration, and diuresis resulted by glucosuria may cause significant electrolyte disturbances with potassium loss.
The risk factors for DKA include newly-diagnosed diabetes, lack of insulin, drug use, and amplified insulin demand due to infections. Lack of insulin could be triggered by the failure of an insulin pump and noncompliance to insulin therapy probably due to psychological factors, altered body image, and financial constraints. The prescription drugs implicated with the occurrence of DKA include risperidone, olanzapine, clozapine, pentamidine, sympathomimetics, interferon, thiazide diuretics, glucagon, and corticosteroids. Alcohol and cocaine as well as trauma, pregnancy, cerebrovascular accidents, acromegaly, Cushing’s disease, arterial thrombosis, pancreatitis, hypovolemic shock, myocardial infarction, psychological stress, and hemochromatosis are also known to cause DKA. Urinary tract infections, pneumonia, and sepsis can cause DKA if they occur concomitantly with type 1 diabetes.
Currently, YS experiences fatigue, nausea and vomiting, abdominal pain, fruity breath, hyperglycemia, and excessive urination. She is alert though slightly drowsy indicating that her DKA is moderate. DKA’s presentation depends on the comorbid conditions and its severity. Polydipsia and polyuria manifest in almost all patients with juvenile-onset diabetes. Other symptoms include fatigue, weight loss, dyspnea, a previous febrile condition, vomiting, polyphagia, and abdominal pain. The loss of fluid through excessive urination causes dehydration. Consequently, the patient presents with poor skin turgor, tachycardia, orthostatic hypotension, and dry mucous membranes. Moreover, the metabolic acidosis caused by ketonemia may trigger a compensatory mechanism by the lungs manifesting as Kussmaul respirations that are characteristically deep (Westerberg, 2013). Elevated acetone titers in the body are detected as they yield a fruity scent on the breath. The patient’s mental status may range from dizziness to lassitude and loss of consciousness.
The severest complication of DKA is cerebral edema. It has a significant mortality rate in as much as it occurs in a small percentage of patients with DKA. Survivors of cerebral edema have a propensity to suffer from lingering neurologic complications (Haringhuizen, Tjan, Grool, van Vugt, & van Zante, 2010). The risk factors for cerebral edema include severe acidosis, younger age, protracted symptoms, newly-diagnosed diabetes, low bicarbonate level, hyponatremia, and hyperglycemia. It is associated with decrease in carbon dioxide partial pressure, fluid retention in stomach, and hurried hydration. Its definitive signs that necessitate immediate assessment are bradycardia, headache, continuous vomiting, hypertension, lethargy, hypoglycemia, acute renal failure, shock, and hypokalemia. Rare occurrences include thrombosis and stroke, pulmonary edema, rhabdomyolysis, memory loss in children, pneumomediastinum, and impaired cognition, especially in pediatric patients (Ghetti, Lee, Sims, Demaster, & Glaser, 2010).
Diagnostic Tests for DKA with Normal Values and Deviations
|Diagnostic Test||Normal Result||Reasons for Abnormal Values|
|Arterial Blood Gases
· O2 saturation
· Base excess
|Low due to metabolic acidosis.
Slightly low due to respiratory compensation of the metabolic acidosis.
A negative number due to metabolic acidosis.
|HbA1c||4-5.6%||The value was elevated due to hyperglycemia and poor glycemic control.|
|Anion gap||8-16 mEq/L||Gap >12 mEq/L due to acidosis.|
|Increased BUN and serum creatinine due to a decrease in GFR and extracellular volume.|
|ECG||Prolonged QT interval, depressed ST segment, and changes in the directions and amplitudes of the T waves due to a hyperglycemic crisis.|
|Serum bicarbonate||22-29 mmol/L||Low due to metabolic acidosis.|
|Serum glucose level||>140 mg/dL||High glucose levels due to inadequate insulin.|
|Complete blood count
· White blood cells
|4.0-12.0 x 103 /µL||Slightly elevated white blood cell count due to the hyperglycemic crisis.|
Medication and Treatments
IV fluid should be initiated following the determination of the extent of dehydration. Initially, the patient is infused with a liter of normal saline hourly. Meanwhile, urine output, electrolyte level, fluid status, blood pressure, and cardiac status are monitored (Westerberg, 2013). On stabilization, the amounts of saline and its concentration are reduced. On attaining glycemic control, dextrose is incorporated. Oral or intravenous fluid replacement helps counter the dehydration caused by polyuria. It dilutes the sugar in blood. However, rapid hydration could cause cerebral edema.
For DKA, insulin is also administered intravenously to reverse the cascades precipitating the hyperglycemic crisis. However, when the blood’s acidity reduces and the glucose levels fall below 240 mg/dL, the intravenous insulin infusion should be halted as the patients can now continue with their regular insulin therapy (Mayo Clinic Staff, 2015a). Subcutaneous insulin can also be used in persons whose DKA is uncomplicated (Westerberg, 2013). Patients with a known history of diabetes resume their outpatient regimens. However, newly-diagnosed diabetics are required to take insulin in divided summing up to 0.5 to 0.8 mg/kg/day (Westerberg, 2013). Insulin therapy could lead to the sudden drop in blood sugar causing hypoglycemia. Rapid adjustment of blood sugar levels could also yield cerebral edema, especially in children like YS who have just been diagnosed with diabetes (Westerberg, 2013). Therefore, insulin is recommended to be administered gradually. Additionally, insulin could precipitate hypokalemia that typically manifests as an impairment of the nerve, heart, and muscle functions.
In the treatment of DKA, the concentration of serum potassium should remain 4-5 mmol/L. Potassium therapy enables neurons, muscles, and heart to function normally. It is necessary to monitor potassium levels every three hours during the initial stages of DKA. Should the potassium concentrations fall in the normal range, therapy can be initiated at a rate of ten to fifteen milliequivalents of potassium per hour. However, care should be taken with the administration of potassium as oversights during monitoring may cause hyperkalemia.
The inclusion of bicarbonate in the treatment of DKA is contentious. However, it is incorporated to counter severe acidosis that could cause neurological and cardiac complications. The American Diabetes Association recommends bicarbonate therapy in individuals whose blood pH is lower than 6.9. Infusion with bicarbonate should be monitored because if it surpasses the physiological range, it will result in metabolic alkalosis.
Phosphate therapy should be initiated if the blood concentrations of the ion are less than 0.32 mmol/L thus preventing cardiac arrhythmias, hemolysis, muscle fatigue, respiratory failure, and rhabdomyolysis associated with phosphate deficiency. Persons with congestive heart failure, respiratory complications, or anemia can benefit from this treatment. The electrolyte is administered by adding about twenty-five milliequivalents of potassium phosphate to the saline for infusion. Blood levels of phosphate should be checked regularly to prevent hyperphosphatemia.
Since the patient has newly diagnosed diabetes, she should consult her primary care doctor to discuss the recommended treatment plan. The patient should also see a registered nurse, who is knowledgeable in managing patients with diabetes, can provide critical care, and advocate for the patient’s interests. Registered dietitians advise on the recommended diet for patients. An endocrinologist advises on hormonal therapy and the appropriate measures to take to maintain hormonal balance. It is important to contact an eye doctor as hyperglycemia affects eyes as it results in the formation of sorbitol causing cataracts.
Diabetes causes peripheral neuropathy, increases the risks of infection, makes joint stiffer, interferes with the body’s healing process, and causes diabetic foot that affects the feet. Such problems can be handled by podiatrist. Exercise is known to improve the sensitivity of the cells to insulin thus control of blood glucose. A newly diagnosed diabetic should seek the counsel of an exercise physiologist on the appropriate physical activities to undertake. The patient should see a pharmacist for advice on the appropriate medicines to take, their side effects, dosages, contraindications, and directions for use. Additionally, a pharmacist can conduct therapeutic drug monitoring to assess the efficiency of treatment and compound extemporaneous medication.
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Nursing Care Plan
With reference to the problem, etiology, and symptoms format, the following would be the patient’s listed diagnoses: fluid volume deficit related to excessive vomiting as evidenced by thirst and a decrease in blood pressure, the risk for infections related to high glucose levels and the risk for electrolyte imbalance associated with the deficient fluid volume. The care plan below will zero in on the priority diagnosis of fluid volume deficit. The management goals for this patient as the disease progresses are to preclude and lessen the fluid volume deficit related to excessive vomiting as evidenced by thirst and decrease blood pressure.
The patient will maintain fluid volume at the functional level as evidenced by a capillary refill less than three seconds, and that blood pressure contained within the normal range. Additionally, she will have a normal skin turgor, pre-prandial blood glucose levels between 70-130 mg/dL and levels less than 180 two hours after starting a meal, and a urinary output greater than 30 ml/hour twenty-four hours after receiving treatment.
The foundational intervention to attain the above-stated goal would be to monitor and record the patient’s vitals to ensure that the blood pressure is maintained within a normal range. Should there be any derangements from the targeted value, the primary care doctor should be informed immediately. Additionally, the patient should be observed for signs of dehydration so that the outcome of maintaining a normal skin turgor is attained. YS’s breathing pattern should be observed as DKA presents with shortness of breath in addition to assessing her level of consciousness to prevent her from developing syncope. Other interventions would include monitoring the patient’s weight, fluid intakes, and output to ensure that the desired outcome is achieved. She should be encouraged to take copious amounts of water along with the intravenous fluid infusion administered to her. It would also be essential to create a comfortable environment that enhances recuperation while monitoring the results of the laboratory tests to ensure that glycemic control is achieved. Ultimately the patient ought to be taught on how to keep her sugar levels under control.
On evaluating the patient on the effectiveness of the interventions, the registered nurse documented the capillary refill and vital signs as required and as noted, the values were within the normal limits and as such, the first and second outcomes were achieved. Evaluation of the patient’s skin reveals that the turgor has reverted to normalcy. However, her urinary output and blood sugar levels are yet to normalize and as documented by the nurse. Since the patient does not meet all her outcomes, the medical team will keep on working with the patient and her family on further interventions and the relevant education that would see into the smooth attainment of the desired results.
Plan for Discharge
YS’s long-term goal is to become successful at self-monitoring for blood glucose levels. As such, her release plan would incorporate lessons on how to use a glucometer and the relevance of the values she records. Further, she should be advised on what to do should she notice a rise in the levels of her blood glucose. Additionally, the patient should be provided with information on how to self-administer insulin and should be taken through the recommended schedule for information, and the dosage. The patient and her family should learn about the dietary requirements and restrictions as stipulated for the subject in addition to advising them to take a keen look at the composition of various foods before serving them to YS. It would be essential to notify the patient on the benefits of exercising regularly. She should, however, remember to check her blood sugar before, during, and after the exercise.
The registered nurse should emphasize the importance of taking in adequate amounts of fluid. Most importantly, the patient should be forewarned about the signs that would necessitate a contact or visit to the provider. YS should look out for a fruity breath, abdominal pains, nausea, vomiting, fever, excessive thirst, and excessive urination. At this point, it would be important to clarify any unclear areas, assess the extent to which the patient has taken in the instructions, and address any other concerns. The patent will then be discharged to go home under the care of her parents once tight glycemic control is achieved. However, since the patient is still of a tender age, there are concerns as to whether she understands the bearing of monitoring her blood glucose and the severity of DKA. It would, therefore, be important that the primary care doctor organizes for routine follow-up visits to enable him/her assess the patient’s progress.