1.0 sugar, low blood pH, and ketoacids in

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Last updated: February 13, 2019

1.0 INTRODUCTIONDiabeticketoacidosis (DKA) is a potentially life-threatening complication of diabetesmellitus. Signs and symptoms may include vomiting, abdominal pain, deep gaspingbreathing, increased urination, weakness, confusion, and occasionally loss ofconsciousness. A person’s breath may develop a specific smell. Onset ofsymptoms is usually rapid.

In some cases people may not realize they previouslyhad diabetes.DKAhappens most often in those with type 1 diabetes, but can also occur in thosewith other types of diabetes under certain circumstances. Triggers may includeinfection, not taking insulin correctly, stroke, and certain medications suchas steroids. DKA results from a shortage of insulin, in response the bodyswitches to burning fatty acids which produces acidic ketone bodies. DKA istypically diagnosed when testing finds high blood sugar, low blood pH, andketoacids in either the blood or urine.Theprimary treatment of DKA is with intravenous fluids and insulin. Depending onthe severity, insulin may be given intravenously or by injection under theskin.

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Usually potassium is also needed to prevent the development of low bloodpotassium. Throughout treatment blood sugar and potassium levels should beregularly checked. Antibiotics may be required in those with an underlyinginfection. In those with severely low blood pH, sodium bicarbonate may begiven, however its use is of unclear benefit and typically not recommended.         2.0 CASE STUDY Mr.

Saifuddin Bin Ab Rahman, 45 years old with underlying Diabetes Mellitus forthe past 8 years ago, on medication metformin and gliclazide. He also had hypertensionsince 4 years ago, on one antihypertensive medication but noncompliance tomedication. Patient under Klinik Kesihatan Tawau follow up. Patient presentedto ED Hospital Sungai Buloh with complaints of upper abdominal pain for fourdays and worsening today. The pain score was 7/10. Not related to meal andnon-radiating. Patient had complaining of vomiting two episodes since todaywith food content, no biles and no blood. Patient also having shortness ofbreath today night, thus came in to ED.

Patient bowel open and urine output isnormal. Patient had reduced oral intake since yesterday. Otherwise, patientdenied of fever, diarrhoea, chest pain, palpitation, slurred speech, bodyweakness, UTI symptoms and URTI symptoms. Patient actually travelled from TawauSabah visiting relatives. However his medication was finished. So he not takes hismedication for the past one week.

 On examination uponarrival in ED, the patient was drowsy;GCS full, peripheries were warm, good pulse volume, capillary refill time lessthan 2 seconds, rapid and deep breathing. Patient looks lethargic. The tonguewas moist. His vital signs were Temperature was 37 Celcius, Pulse rate was 125bpm, Respiration rate was 30/min, Blood pressure was 137/86 mmHg, MAP: 99 mmHgand Sp02 was 98% under room air. Auscultation on lungs showed equal and clearair entry. Cardiovascular system showed dual rhythm no murmur. Examination onabdomen showed soft tenderness over epigastric, right hypochondriac and lefthypochondriac region.

 Investigation that hadbeen done to Mr. Saifuddin includes Full Blood Count (FBC). The results were Hb20.6 / Hct 58 / WCC 16.7 / Platelet 329. The result of Venous Blood Gases were pH7.

037 / HC03 8.4 / lactate 5.3 / BE -21 / glucose 54 / Potassium (K) 4.9 / Sodium(Na) 129. The urine ketone was 4.8.

Capillary blood glucose was high. ECGshowed sinus tachycardia. The impressionfor Mr Saifuddin was Diabetic Ketoacidosis secondary to noncompliance tomedication. The plan management forthis patient at resus with weight of 84 kg were High flow mask 15L/min. IV dripnormal saline 20cc/kg/hour. IV infusion insulin 0.1mg/kg/hour.

Insertion of CBD.Sent for chest X-ray. Monitor the vitals sign and Dextrostix hourly.

                              3.0 DISCUSSION From the case study above, it is clearthat Mr. Saifuddin is underlying of hypertension and diabetes mellitus.

Patientactually travelled from Tawau Sabah visiting relatives. However his medicationwas finished. So he not takes his medication for the past one week. Thisconsiders the patient has miss medication leads to serious complication whichis diabetic ketoacidosis (DKA). The symptoms like abdominal pain, vomiting andloss of appetite that he had can consider that he had complication of hisdiabetes.  Diabetic ketoacidosis(DKA) is a complex disordered metabolic state characterised by hyperglycaemia,acidosis, and ketonaemia.

DKA usually occurs as a consequence of absolute orrelative insulin deficiency that is accompanied by an increase incounterregulatory hormones (ie, glucagon, cortisol, growth hormone,epinephrine). This type of hormonal imbalance enhances hepatic gluconeogenesisand glycogenolysis resulting in severe hyperglycaemia. Enhanced lipolysisincreases serum free fatty acids that are then metabolised as an alternativeenergy source in the process of ketogenesis. This results in accumulation oflarge quantities of ketone bodies and subsequent metabolic acidosis. Ketonesinclude acetone, 3-beta-hydroxybutyrate, and acetoacetate.

The predominantketone in DKA is 3-betahydroxybutyrate (Caputo, D.G. 2010). According to Kitabchi,A.E.& Nyenwe, E.A. (2006), DKA consists of the biochemical triad ofketonaemia/ ketonuria, hyperglycaemia, and acidaemia.

From the above casestudy, Mr. Saifuddin showed ketone in his urine as the result of urine ketonewas 4.8. Patient’s capillary blood glucose was high and from the result ofvenous blood gas (VBG), the glucose was 54.

Patient is hyperglycaemia. Theresult of VBG also showed the patient had acidosis which the pH was 7.037 andHC03 was 8.

4. From all the investigation carried out to Mr. Saifuddin, itshowed that he is diagnosed with Diabetes Ketoacidosis and must be treatingpromptly. There are severalmechanisms responsible for fluid depletion in DKA. These include osmoticdiuresis due to hyperglycaemia, vomiting commonly associated with DKA, andeventually, inability to take in fluid due to a diminished level ofconsciousness.

Electrolyte shifts and depletion are in part related to theosmotic diuresis. Hyper and hypokalaemia need particular attention.              Accordingto Devalia, B. (2010) the therapeutic goals of DKA management includeoptimization of volume status, hyperglycemia and ketoacidosis, electrolyteabnormalities; and potential precipitating factors. The majority of patientswith DKA present to the emergency room. Therefore, emergency physi­cians shouldinitiate the management of hyperglycemic crisis while a physical examination isperformed, basic metabolic parameters are obtained, and final diagnosis ismade. Several important steps should be followed in the early stages of DKAmanagement. First of all, collect blood for metabolic profile before initiationof intravenous fluids.

Then, infuse 1 L of 0.9% sodium chloride over 1 hourafter drawing initial blood samples. Next, ensure potassium level of >3.

3mEq/L before initiation of insulin therapy (supplement potassium intravenouslyif needed). Lastly is initiate insulin therapy.             Bloodglucose is routinely checked at the bedside, but portable ketone meters nowalso allow bedside measurement of blood ketones (3-betahydroxybutyrate). Thisis an important advance in the management of DKA (Sheikh-Ali, 2008). Theresolution of DKA depends upon the suppression of ketonaemia, thereforemeasurement of blood ketones now represents best practice in monitoring the responseto treatment. Access to blood gas and blood electrolyte measurement is nowrelatively easy and available within a few minutes of blood being taken.Therefore glucose, ketones and electrolytes, including bicarbonate and venouspH should be assessed at or near the bedside.

             Themost important initial therapeutic intervention in DKA is appropriate fluidreplacement followed by insulin administration. The main aims for fluidreplacement are restoration of circulatory volume, clearance of ketones andcorrection of electrolyte imbalance. For example, an adult weighing 70kgpresenting with DKA may be up to 7 litres in deficit. This should be replacedas crystalloid. In patients with kidney failure or heart failure, as well as theelderly and adolescents, the rate and volume of fluid replacement may need tobe modified. The aim of the first few litres of fluid is to correct anyhypotension, replenish the intravascular deficit, and counteract the effects ofthe osmotic diuresis with correction of electrolyte disturbance (Nyenwe, E.A.

& Kitabchi, A.E. 2011).             For Insulin therapy a fixed rate calculatedon 0.1 units/ per kilogram infusion is recommended.

It may be necessary to estimatethe weight of the patient. Insulin has the following effects such assuppression of ketogenesis, reduction of blood glucose and correction ofelectrolyte imbalance. The metabolic treatment targets include reduction of theblood ketone concentration by 0.5 mmol/L/hour, increase the venous bicarbonateby 3 mmol/L/hour, reduce capillary blood glucose by 3 mmol/L/hour, potassiumshould be maintained between 4.0 and 5.0 mmol/L. If these rates are not achievedthen the fixed rate IV insulin infusion rate should be increased (Randall, L.

,Begovic, J., Hudson, M., et al. 2011). According to Umpierrez,G.E.

, Smiley, D. & Kitabchi, A.E. (2012) the management of intravenousglucose concentration should be focussed on clearing ketones as well as normalisingblood glucose. It is often necessary to administer an intravenous infusion of10% glucose in order to avoid hypoglycaemia and permit the continuation of afixed rate IV insulin infusion to suppress ketogenesis.

Introduction of 10%glucose is recommended when the blood glucose falls below 14 mmol/L. It is importantto continue 0.9% sodium chloride solution to correct circulatory volume. It maybe necessary to infuse these solutions concurrently.

Glucose should not be discontinueduntil the patient is eating and drinking normally.            4.0  NURSING CONSIDERATION An important part of theplan is the nursing diagnosis. It is made based on the assessment of themedical history, symptoms, drugs administered and clinical assessment. In thiscase, the condition due to diabetic ketoacidosis is a fluid volume deficit,metabolic acidosis, excessive blood glucose levels, high potassium levels,dehydration, along with imbalances in nutrition, infection related to the influenzaand fatigue. The key nursing diagnoses include high blood glucose related toinsulin deficiency as manifest by diabetic ketoacodosis. Besides, dehydrationrelated to hyperglycemia as manifest by frequent urination, weakness and dryskin also important in nursing diagnosis.

Other nursing diagnosis potassium imbalancerelated to osmotic diuresis as manifest by unstable vital signs, cramps andmuscle weakness. Lastly, metabolic acidosis related to ketones presence inblood as manifest by kussmul’s breathing, nausea, confusion and drowsiness.The assessmentwould include the airway, breathing, circulation (dehydration) and theneurological state. There is an osmotic diuresis related to hyperglycemiacausing excessive gastric losses in the form of vomiting, abdominal pain anddiarrhea, and lowered intake of food (nausea and sub-consciousness). Thesensory perception of the patient is also altered due endogenous chemicalalterations. Evidence for making the nursing diagnosis is done based on thepresence of symptoms/features such as great output of urine, diluted urine,excessive thirst, sudden loss of body weight, poor food intake, diarrhea andvomiting, altered neurological state, rise in the ketone levels in the bloodand the urine, lowered blood pressure and increased heart rate, Kussmaul’srespiration (deep and rapid breathing), and dry and cracked skin with poorturgor.

        5.0 SUMMARYHyperglycemia andketosis in diabetic ketoacidosis (DKA) are the result of insulin deficiency andan increase in the counterregulatory hormones glucagon, catecholamines,cortisol, and growth hormone. Three processes are mainly responsible forhyperglycemia: increased gluconeogenesis, accelerated glycogenolysis, andimpaired glucose utilization by peripheral tissues. This might also beaugmented by transient insulin resistance due to hormone imbalance, as well aselevated free fatty acids.DKA is most commonly precipitated by infections. Other factorsinclude discontinuation of or inadequate insulin therapy, pancreatitis,myocardial infarction, cerebrovascular accident, and illicit drug use. Thediagnostic criteria of DKA, established by the American Diabetic Association,consists of a plasma glucose of >250 mg/dL, positive urinary or serumketones, arterial pH of <7.3, serum bicarbonate <18 mEq/L, and a highanion gap.

The key diagnostic feature of DKA is elevated circulating totalblood ketone concentration. Hyperglycemia is also a key diagnostic criterion ofDKA; however, a wide range of plasma glucose levels can be present onadmission.               References Caputo, D.G., Villarejo, F., Valle, G.

B.,Díaz, A.P., Apezteguia, C.J. (2010).

Hydration in diabetic ketoacidosis. Whatis the effect of the infusion rate? Medicina (B Aires) 2010;57(1):15–20.Devalia, B. (2010). Adherance to protocolduring the acute management of diabetic ketoacidosis: would specialistinvolvement lead to better outcomes? Int J Clin Pract. 64(11):1580–1582.

Gosmanov, A.R., Umpierrez, G.E.

, Karabell,A.H., Cuervo, R., Thomason, D.

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, Nyenwe, E.A. (2006).Hyperglycemic crises in diabetes mellitus: diabetic ketoacidosis andhyperglycemic hyperosmolar state. Endocrinol Metab Clin North Am.

35(4):725–751.Kitabchi, A.E., Umpierrez, G.E., Murphy, M.

B.,Kreisberg, R.A. (2006). Hyperglycemic crises in adult patients with diabetes: aconsensus statement from the American Diabetes Association. Diabetes Care.

29(12):2739–2748. Nyenwe, E.A., Kitabchi, A.E. (2011).

Evidence-basedmanagement of hyperglycemic emergencies in diabetes mellitus. Diabetes ResClin Pract. 94(3):340–351.Randall, L., Begovic, J., Hudson, M., etal. (2011).

Recurrent diabetic ketoacidosis in inner-city minority patients:behavioral, socioeconomic, and psychosocial factors. Diabetes Care. 34(9):1891–1896.Sheikh-Ali, M., Karon, B.S., Basu, A.

, etal. (2008). Can serum beta-hydroxybutyrate be used to diagnose diabetic ketoacidosis? DiabetesCare. 31(4):643–647. Umpierrez, G.

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Narrative review: ketosis-prone type 2 diabetes mellitus. AnnIntern Med. 144(5):350–357.

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