Gretchen Crabtree, AG-ACNP - Home



Comprehensive Clinical Case Study: Diabetic KetoacidosisGretchen CrabtreeWright State UniversityHistory and PhysicalSourceMother via telephone, who is a reliable historian and roommate who is present at the bedside. Chief ComplaintAltered mental status and nausea and vomiting. History of Present IllnessEighteen year old patient presents to the emergency department via squad after his roommate came home from class and found the patient barely responsive on the bathroom floor in a pile of vomit. Patient would only moan to speech, so the squad was called. Mother states the patient is prescribed regular insulin through primary care provider, but does not know the administration regimen because the patient has been managing it himself since the age of fourteen. Roommate states he has not seen the patient take any insulin for approximately three days. Past Medical HistoryDiabetes mellitus type I, diagnosed at the age of eleven. Past Surgical HistoryNoneFamily History Mother is living at age 52 with no medical history. Father is living at age 54 with no medical history. One younger brother and one younger sister living without medical problems. Social HistoryPatient is a single, freshman college student. Roommate states the patient does not smoke. Roommate states he does drink two to three nights a week, about 12 beers each time. He states he does not use recreational drugs to the roommate’s knowledge. Patient is not employed. Mother states the patient has not had any recent travel or exposures. MedicationsUnknown amount of regular insulin. SubjectivePatient is unable to give subjective information at this time, other than what is noted in HPI per roommate. ObjectiveData: Temp 99.7 BP 95/62 HR 128 RR 32 oxygen saturation 94% on room air. Height 71 inches and weight 95.3kg. Lab ResultsTable 1. Complete Blood CountResultsNormal RangeWBC11.74.8-10.8 x103x mcLRBC5.994.7-6.1 x 106/mcLHemoglobin17.613.6-17.5 g/dLHematocrit53.839-49%MCV89.780-110 fLMCH29.327-34 pgMCHC32.731-36g/dLRDW13.311.5-14.5%Platelets251150-450 x103/mcLLymphocytes1.10.8-3.5 x 103/mcLNeutrophils10.32.2-8.6 x 103/mcLMonocytes0.30.2-0.8 x 103/mcLEosinphils0.00.04-0.5 x 103/mcLBasophils0.00.01-0.12 x 103/mcL(Merck Manual, 2013)Table 2. Basic Metabolic PanelResultsNormal ValuesSodium137135-145 mEq/LPotassium5.63.5-5.0 mEq/LChloride96101-112 mEq/LCarbon Dioxide922-32 mEq/LGlucose70460-110 mg/dLBUN378-20mg/dLCreatinine1.810.6-1.2 mg/dLGFR53Calcium11.08.5-10.5 mg/dLOsmolality 326280-300KetonesPositive (Large)NegativeSalicylate NegativeNegativeEthanol level0<10mg/dLMethanol level0<10mg/dL (Merck Manual, 2013)Table 3. Arterial Blood GasResultsNormal ValuepH7.107.32-7.44pCO22835-45mmHgpO29785-104mmHgBase Excess-18.6-2.0-3.0 mEq/LHCO38.921-27 mEq/LSpO29495-98%(Merck Manual, 2013)Table 4. UrinalysisResultsNormal ValueColorLight yellowYellowClarityClearClearGlucose, urine>1000Normal mg/dLBilirubin, urineNegativeNegative mg/dLKetone, urine150Negative mg/dLSpecific gravity1.0201.010-1.025Blood, urineNegativeNegativepH, urine5.05.0-8.0Protein, urine25Negative <20 mg/dLUrobilinogenNormalNormalNitrite, urineNegativeNormal mg/dLLeukoesteraseNegativeNegativeUrine microFew epithelial cells, few bacteria, 0-3 WBC/hpf(Merck Manual, 2013)Table 5. Urine Drug ScreenResultsNormal valuePhencyclidineNegativeNegativeBenzodiazepinesNegativeNegativeCocaineNegativeNegativeAmphetamineNegativeNegativeCannabis (THC)NegativeNegativeOpiatesNegativeNegativeBarbituratesNegativeNegativeECG showed sinus tachycardia without ectopy or ST changes noted. HChest x-ray: the lungs are clear and the heart and mediastinum and pulmonary vascularity are normal. No acute cardiopulmonary abnormality. Physical Exam: GENERAL APPEARANCE: Appears ill, lying in bed barely arousable. PSYCH: Unable to assess. NEUROLOGICAL: Unable to assess orientation. Pupils are pinpoint, equal, reactive to light. Patient moans to speech and is able to localize pain. HEENT: Conjunctivae and lids are within normal limits. Neck within normal limits. No palpable masses. Thyroid is within normal limits. Dry mucous membranes. Fruity odor to breath. RESPIRATORY: Bilateral chest expansion and symmetrical. Respirations are shallow and tachypnea is present. Lungs are clear to auscultation bilaterally. HEART: S1/S2 noted, regular heart rhythm, tachycardic. ECG was reviewed. Sinus tachycardia without ectopy or ST changes. Right lower extremity does have 2+ dorsalis pedis and 2+ posterior tibialis pulses. Left lower extremity does have2+ dorsalis pedis and 2+ posterior tibialis pulses. No edema noted. GI: Abdomen is soft, nontender, nondistended, symmetrical, positive bowel sounds x 4 quadrants. MUSCULOSKELETAL: Unable to assess muscle strength. No atrophy noted. SKIN: Pink, warm, dry, intact without any abnormalities.Differential DiagnosisTable 6. Probability of DiagnosisDifferential DiagnosisHallmark symptoms and findingsDegree of probabilitySalicylate ingestionSymptoms include tachypnea with increase in depth and rate, renal excretion of potassium and bicarbonate, hallucinations, confusion, convulsions, loss of consciousness (in severe cases), hypertension, tachycardia, tinnitus, nausea, vomiting, and fever. The patient can also have respiratory alkalosis and metabolic acidosis (Kumar & Clark, 2012). There is a moderate probability the patient has salicylate toxicity. Many of the symptoms are similar and could explain the patient’s condition. However, once blood work is drawn, the clinician is able to rule it out since the salicylate level was zero. Ethylene glycol ingestionSymptoms present in different stages after time of ingestion. Once the glycoaldehyde forms approximately four to twelve hours later seizures, coma, and nausea and vomiting. After 12-24 hours cardiorespiratory symptoms occur including tachypnea, tachycardia, hypo/hypertension, congestive heart failure, pulmonary edema, calcium oxalate crystals in the lungs, myocardium, or meninges. Then 24-72 hours later the damage to the kidneys presents. The patient will have a metabolic acidosis with elevated anion gap (Kumar & Clark, 2012). There is a low probability the patient has ethylene glycol ingestion. His presenting symptoms are similar in nature and he does have a metabolic acidosis with an elevated anion gap. However, based on his laboratory findings his blood alcohol level was negative. Methanol ingestionThe symptoms of methanol poisoning may not become apparent for the first 72 hours after exposure. If ingested can lead to agitation, decreased level of consciousness, headache, dizziness, nausea, vomiting, anorexia, diarrhea, visual disturbances, photophobia, electrolyte imbalances, kidney failure, hematuria, rhabdomyolysis, tachycardia, and tachypnea (Kumar & Clark, 2012).There is a low probability the patient has methanol ingestion. Based on the roommate and mother’s knowledge the patient has not had exposure to methanol. Also only a small amount of the symptoms are similar in nature. Lastly the patient’s lab work shows a negative blood methanol level. Diabetic Ketoacidosis (DKA) The presenting symptoms of DKA are tachycardia, hypotension, hyperventilation, nausea, vomiting, altered mental status, evidence of dehydration, fruity breath, cool and dry skin. In severe cases patient may be in a stupor or even coma. Findings on labs include hyperglycemia, metabolic acidosis, large amount of ketones in blood and urine, and elevated anion gap (Kumar & Clark, 2012).There is a high probability the patient has DKA. This determination is based on the history of the patient being a type I diabetic, symptoms, and laboratory findings. The symptoms include tachycardia, hypotension, altered mental status, nausea, vomiting, and hypovolemia. The patient also has hyperglycemia, metabolic acidosis, and an anion gap of 32. Diagnostic testingA patient who presents to the emergency department with altered level of consciousness via squad should have baseline laboratory tests drawn. A complete blood count with differential is completed to evaluate white blood cell count, hemoglobin, and platelet count. Elevations in white blood cell count can detect sepsis, a possible cause of DKA. A complete metabolic profile is also performed to evaluate hyperglycemia, electrolyte imbalances and to determine the severity of DKA and measure anion gap. Another aspect in the diagnosis of DKA is metabolic acidosis. In order to assess the extent an arterial blood gas needs to be drawn. If available a beta-hydroxybutyric acid level should be drawn as well. Beta-hydroxybutyric acid can be drawn to help detect patients at high risk for DKA who present with hyperglycemia with a higher specificity and sensitivity. A rapid urine drug screen needs to be completed to rule out any type of overdose or intoxication, which may be the cause of unresponsiveness and can lead to DKA (Goguen & Gilbert, 2013). Table 7. Diagnostic criteria and water and electrolytes deficits.Mild DKAModerate DKASevere DKADiagnostic criteria and classificiationPlasma glucose>250>250>250Arterial pH7.25-7.307.0-7.24<7.0Serum bicarbonate15-1810-15<10Urine ketonePositivePositivePositiveSerum ketonePositivePositivePositiveAnion gap>10>12>12Mental statusAlertAlert/drowsyStupor/ComaTypical deficitsTotal water6 LitersWater (ml/kg)100Sodium (meq/kg)7-10Chloride (meq/kg)3-5Potassium (meq/kg)3-5pO2 (mmol/kg)5-7Magnesium (meq/kg)1-2Calcium (meq/kg)1-2(Nyenwe & Kitabchi, 2011) A chest radiograph is recommended to rule out any aspiration due to the patient lying in his vomit when the roommate found him. It is a cost effective way to ensure there is not an underlying respiratory process. According to Healthcare Blue Book a fair price for a chest radiograph is $44. It has a sensitivity of 65-85% and specificity of 85-95%. A computed topography of the head should be included as well to rule out any intracranial process. Since the patient presented with unresponsiveness which can be associate with DKA, however there still could be another neurological cause. This is the reason it is important to get a CT of the head (Goguen & Gilbert, 2013). Prioritized planThere are several priorities when managing a patient with DKA including fluid resuscitation, correcting hyperglycemia and electrolyte imbalances, reversing the ketoacidosis, and treatment of any underlying illness. In this case, the underlying cause is assumed to be the patient not taking his insulin as prescribed. Fluid resuscitation and insulin therapy needs to be first administered in the emergency department and continued in the intensive care unit (ICU). This is an appropriate placement for this patient given his mental status and severity of DKA. Typical length of stay in the ICU is approximately 24 hours and then the patient is transferred to the step down floor once the anion gap has closed and there are no longer ketones present. In the emergency department, if the patient is continuing to experience nausea and vomiting the patient should have a nasogastric tube placed to prevent further aspiration. Once the patient is more conscious and hyperglycemia has been corrected the nasogastric tube can be removed (Goguen & Gilbert, 2013).According to the guidelines, initial fluid resuscitation should be corrected in the first twenty four hours. It should start with isotonic saline at rate of 15-20ml/kg/hr during the first hour then tailored to the subsequent labs, hemodynamic status, signs of hydration, and serum electrolytes. Corrected serum sodium is calculated by adding 1.6mmol/L of sodium for every 100mg/dL of glucose above 100mg/dL. Typically 0.45% saline at 250-500ml/hour is sufficient. However, if hyponatremia is still present normal saline should be continued at the rate of 250-500ml/hour. Once the blood glucose level is less than 200-250mg/dL, 5% dextrose should be added to the intravenous fluid in order to prevent hypoglycemia. Twenty four hours after the fluid resuscitation was started the patient should be adequately resuscitated. The average volume deficit is seven liters (Nyenwe & Kitabchi, 2011). Recommendations for adequate reversal and normalization of hyperglycemia include an intravenous insulin regimen. An initial bolus of 0.1 units/kg should be administered followed by a drip rate of 0.1 unit/kg/hour. The glucose level should decrease by approximately ten percent in the first hour. If this is not the case another bolus of insulin can be given at the same dose. It is important to not decrease the serum glucose too fast due to electrolyte and fluid shifts within the vasculature system and can cause cerebral edema. Once the blood sugar is 200-250, the drip rate should be decreased to 0.02-0.05 unit/kg/hour with the addition of dextrose to the intravenous fluid. It is important to keep the glucose high enough to be able to keep the insulin infusing. This is typically between 150-200mg/dL. Serial basic metabolic panels should be drawn every two hours until the anion gap is closed (value less than 12). Once it has closed and the patient is conscious enough to eat, the patient’s diet may advance as tolerated. The insulin should be switched to subcutaneous insulin with a basal insulin requirement and a short acting insulin with meals (Nyenwe & Kitabchi, 2011). In the presence of DKA there can be pseudo electrolyte abnormalities. This is due to the electrolyte and fluid shifts into and out of the cell during the disease process. Initially there is a pseudo-hyperkalemia and in patients who do not have renal compromise should be given potassium chloride replacement if potassium level is below 5.3meq/L. According to the guidelines approximately 20-30meq should be added to each liter of fluid given to the patient. During DKA the patient may have severe metabolic acidosis. In certain cases bicarbonate can be administered to help correct this abnormality. If the pH is less than 7.0, one to two ampules of sodium bicarbonate can be given until the pH is greater than 7.0. Other cases when it is important to give sodium bicarbonate and the pH is greater than 7.0 are bicarbonate level less than ten or pCO2 less than 12 (Nyenwe & Kitabchi, 2011).In the article written by Goguen and Gilbert, there is an easy to follow algorithm to help guide the treatment of patients with DKA. (Goguen & Gilbert, 2013).The follow up for this patient upon discharge would be with his primary care provider or endocrinologist within a week after discharge to ensure he is receiving an adequate insulin regimen to meet his needs. Since the patient has not had a previous experience with DKA, he will likely be able to return to his previous regimen. Health promotionIn this case the best health promotion for the patient is to ensure he understands the need to continue his insulin regimen daily. It is important to not deviate from the regimen unless instructed by a physician. If the patient has not seen a diabetes educator within the last year, it is helpful for him to have an appointment with one on a yearly basis. It will reinforce the teaching and any further education which can be beneficial to him. A proper diet, low in carbohydrates and sugars and regular exercise will help keep his diabetes under control. Further education on type I diabetes mellitus can be helpful as well. Ensure the patient knows as a type I diabetic insulin is a daily requirement to meet the body’s metabolic needs (Kumar & Clark, 2013). ReferencesHealthcare Blue Book. (2013). Retrieved from , J. & Gilbert, J. (2013) Hyperglycemic Emergencies in Adults. Canadian Journal of Diabetes,37 p S72-S76.Kumar, P. & Clark, M. (2012). Kumar & Clark's Clinical Medicine (8th ed.) New York, NY: Saunders-Elsevier.Merck Manual (2013). Blood Tests: Normal Values. Retrieved from , E.A. & Kitabchi, A.E. (2011). Evidence-based management of hyperglycemic emergencies in diabetes mellitus. Diabetes Research and Clinical Practice, 94 p 340-351. doi: 10.1016/j.diabres.2011.09.012. ................
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