DOCSLIB.ORG

Emergency Management of Diabetic Ketoacidosis in Adults R D Hardern, N D Quinn

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Emergency Management of Diabetic Ketoacidosis in Adults R D Hardern, N D Quinn 210 REVIEW Emerg Med J: first published as 10.1136/emj.20.3.210 on 1 May 2003. Downloaded from Emergency management of diabetic ketoacidosis in adults R D Hardern, N D Quinn ............................................................................................................................. Emerg Med J 2003;20:210–213 The authors propose a regimen for managing diabetic cause serious diagnostic difficulty where the ketoacidosis in adults based on available evidence and patient is unconscious or DKA is the first presen- tation of diabetes (a past history of diabetes mel- their experince in the emergency department. litus will be absent in 1 in 10 patients). The possi- .......................................................................... bility of DKA (or other metabolic acidosis) should be considered whenever assessing a patient who presents with “hyperventilation”4 and it is always iabetic ketoacidosis (DKA) is a potentially essential to measure the blood glucose early in the fatal metabolic disorder presenting most resuscitation of any unconscious patient. weeks in most accident and emergency D 1 Polyuria, polydipsia, and weakness are usually (A&E) departments. The disorder can have present. Nausea, vomiting, or abdominal pain significant mortality if misdiagnosed or mis- may predominate. If the patient is already being treated. Numerous management strategies have treated with insulin, there may be a history of been described. Our aim is to describe a regimen reduced or omitted insulin. Chest pain may be that is based, as far as possible, on available described if DKA complicates acute myocardial evidence but also on our experience in managing infarction, although silent infarction may occur. patients with DKA in the A&E department and On examination the patient has an increased on inpatient wards. depth and rate of respiration. The mouth, tongue A literature search was carried out on Medline and lips are dry. The majority of doctors can smell and the Cochrane Databases using “diabetic ketones on the patient’s breath but this is an ketoacidosis” as a MeSH heading and as text- unreliable sign. There may be other signs of word. High yield journals were hand searched. volume depletion. Signs of infection (for example, Papers identified were appraised in the ways lobar pneumonia) should be sought; absence of described in the Users’ guide series published in fever does not exclude infection. JAMA. We will not be discussing the derangements in http://emj.bmj.com/ intermediary metabolism involved, nor would we Bedside tests suggest extrapolating the proposed regimen to A capillary glucose measurement should be made children. Although some of the issues discussed (ensure there is no sugar on the skin where skin may be considered by some to be outwith the prick is made). remit of A&E medicine it would seem prudent to Defining DKA as serum glucose >250 mg/dl ensure that A&E staff were aware of the probable (>14 mM), metabolic acidosis with corrected pH<7.30 or serum bicarbonate <15 mM and management of such patients in the hours after on September 28, 2021 by guest. Protected copyright. they leave the A&E department. ketonaemia, the sensitivity of urine ketone dip test for ketonaemia in patients with DKA is 97% 5 AETIOLOGY AND DEFINITION (95% CI 92% to 99%). The absence of ketonuria makes the diagnosis of DKA unlikely. It is possible DKA may be the first presentation of diabetes. that clinical staff in the study were using negative Insulin error (with or without intercurrent urine dip stick test to rule out DKA; the study illness) is the most common precipitating factor, would therefore overestimate its sensitivity. Few accounting for nearly two thirds of cases (exclud- laboratories offer an urgent ketone level; an esti- ing those where DKA was the first presentation of mate of the severity of ketonaemia can be made diabetes mellitus).2 from the anion gap (available immediately on The main features of DKA are hyperglycaemia, some “blood gas analysers”); an anion gap >20 metabolic acidosis with a high anion gap and mM is abnormal. See end of article for heavy ketonuria (box 1). This contrasts with the authors’ affiliations Acute myocardial infarction can precipitate other hyperglycaemic diabetic emergency of ....................... DKA. A 12 lead ECG should be recorded. hyperosmolar non-ketotic hyperglycaemia where Correspondence to: there is no acidosis, absent or minimal ketonuria Dr R D Hardern, but often very high glucose levels (>33 mM) and Department of Accident 3 and Emergency Medicine, very high serum sodium levels (>150 mM). Box 1 The usual features of diabetic The General Infirmary, ketoacidosis Great George Street, Leeds DIAGNOSIS LS1 3EX, UK; • Hyperglycaemia (>14 mM). richard.hardern@ Clinical findings • Metabolic acidosis (pH<7.35 and bicarbo- leedsth.nhs.uk There are no specific clinical signs that confirm or nate <15 mM). refute the diagnosis of DKA. The diagnosis is Accepted for publication • High anion gap. 12 December 2001 comparatively straight forward where there is a • Ketonaemia/heavy (3+) ketonuria. ....................... clear history that the patient has diabetes but can www.emjonline.com Diabetic ketoacidosis 211 Box 2 Key points in diagnosis of DKA Box 3 Key points in treatment Emerg Med J: first published as 10.1136/emj.20.3.210 on 1 May 2003. Downloaded from • There are no specific physical symptoms or signs • Get experienced help • Rule out DKA and other causes of metabolic acidosis before • Obtain good venous access and send off blood samples making a diagnosis of hysterical hyperventilation • Consider nasogastric tube if patient not alert • Check capillary blood glucose early but always follow this • Consider urinary catheter if haemodynamically unstable with a formal venous blood glucose level • 0.9% saline 500 ml/h for four hours then 250 ml/h until • Test urine for ketones euvolaemic is an effective fluid regime (unless the patient is • Arterial blood is NOT needed as routine shocked at presentation) • Blood potassium levels should be measured hourly (hyper- • Insulin, by continuous intravenous infusion at 0.1 unit/ kalaemic and hypokalaemic cardiac arrest are common kg/h. The fall in [glucose] should not exceed 5 mM/h. causes of death in patients with DKA2) • Start potassium supplementation after insulin treatment once • Venous blood glucose should be measured hourly during [K+] is below the upper limit of the reference range. insulin infusion • The administration of bicarbonate does NOT increase bio- • A chart should be started to continuously record vital signs, chemical or clinical recovery. urine output, and the results of all tests. saline is the fluid usually used in the initial management of Special tests DKA though no formal comparisons with 0.45% saline or It is not necessary to take arterial blood as a routine in Ringer’s solution have been reported. Volume status can be suspected DKA; venous blood can be sampled in a pre- assessed on the basis of clinical assessment (such as heart rate heparinised syringe and then analysed with a “blood gas ana- and BP), from urine output (a high urine output may indicate lyser”. The mean difference between arterial and venous pH in only osmotic diuresis but a low urine output should trigger a DKA is 0.03 (CI not given in text, but in only 1 case of 44 was 6 thorough assessment of renal function and the state of hydra- the difference greater than 0.1). Arterial sampling should be tion), from urea measurements, and (sometimes) from reserved for cases when respiratory failure is suspected. invasive monitoring. Despite a significant reduction in total body potassium, the In patients with significant comorbidity (especially cardiac serum concentration is usually normal or high at presentation disease) invasive haemodynamic monitoring may help to because of a shift into the extracellular compartment. The guide the rate of fluid replacement. This has not been steepest decline of [potassium] occurs in the first few hours of subjected to prospective evaluation and the potential compli- treatment; many recommend that values are checked at least cations of attempted central cannulation in volume depleted hourly during this phase. patients should be borne in mind. This is not a group of Venous glucose should be measured hourly. Management patients in which to “practise” central cannulation. should be based on capillary glucose measurements only after Once [glucose] has fallen to around 14 mM (a value based these have been found to agree with venous levels (at presen- on tradition more than anything else) 5% dextrose (with tation the degree of hyperglycaemia may render the capillary appropriate potassium) is given rather than saline. Adminis- measurement inaccurate). tering hypertonic dextrose (1 litre 10% dextrose + 40 units Leucocytosis is usual and should not be interpreted as a sign insulin at 250 ml/h) rather than isotonic dextrose (1 litre 5% http://emj.bmj.com/ of infection. Routine treatment with antibiotics is not dextrose + 10 units insulin at 250 ml/h) may accelerate the indicated; blood and urine should be cultured. clearance of ketone bodies but also causes a rise in [glucose] without an additional improvement in blood pH or TREATMENT bicarbonate.8 DKA is a complex life threatening problem and the management should not be left to inexperienced staff. There Insulin should be early consultation between A&E staff and specialist Type of insulin diabetes teams. Patients with DKA need four things; A soluble insulin is normally used with the aim of permitting on September 28, 2021 by guest. Protected copyright. • Fluid more rapid titration of circulating insulin levels (though there • Insulin are no trial data comparing soluble against other types of insulin). If an intravenous bolus is followed by an intravenous • Potassium infusion steady state insulin levels are reached very quickly. • Education The half life of circulating insulin is five minutes; use of an Early venous access is essential. In shocked patients large intravenous infusion has the advantage over intermittent bore cannulas should be sited and standard measures boluses of permitting a more rapid reduction in insulin level.
Load more

Recommended publications
  • Diabetic Ketoacidosis and Hyperosmolar BMJ: First Published As 10.1136/Bmj.L1114 on 29 May 2019
    STATE OF THE ART REVIEW Diabetic ketoacidosis and hyperosmolar BMJ: first published as 10.1136/bmj.l1114 on 29 May 2019. Downloaded from hyperglycemic syndrome: review of acute decompensated diabetes in adult patients Esra Karslioglu French,1 Amy C Donihi,2 Mary T Korytkowski1 1Division of Endocrinology and Metabolism, Department of ABSTRACT Medicine, University of Pittsburgh, Pittsburgh, PA, USA Diabetic ketoacidosis and hyperosmolar hyperglycemic syndrome (HHS) are life threatening 2University of Pittsburgh School of complications that occur in patients with diabetes. In addition to timely identification of the Pharmacy, Pittsburgh, PA, USA Correspondence to: M Korytkowski precipitating cause, the first step in acute management of these disorders includes aggressive [email protected] administration of intravenous fluids with appropriate replacement of electrolytes (primarily Cite this as: BMJ 2019;365:l1114 doi: 10.1136/bmj.l1114 potassium). In patients with diabetic ketoacidosis, this is always followed by administration Series explanation: State of the of insulin, usually via an intravenous insulin infusion that is continued until resolution of Art Reviews are commissioned on the basis of their relevance to ketonemia, but potentially via the subcutaneous route in mild cases. Careful monitoring academics and specialists in the US and internationally. For this reason by experienced physicians is needed during treatment for diabetic ketoacidosis and HHS. they are written predominantly by Common pitfalls in management include premature termination of intravenous insulin US authors therapy and insufficient timing or dosing of subcutaneous insulin before discontinuation of intravenous insulin. This review covers recommendations for acute management of diabetic ketoacidosis and HHS, the complications associated with these disorders, and methods for http://www.bmj.com/ preventing recurrence.
    [Show full text]
  • Persistent Lactic Acidosis - Think Beyond Sepsis Emily Pallister1* and Thogulava Kannan2
    ISSN: 2377-4630 Pallister and Kannan. Int J Anesthetic Anesthesiol 2019, 6:094 DOI: 10.23937/2377-4630/1410094 Volume 6 | Issue 3 International Journal of Open Access Anesthetics and Anesthesiology CASE REPORT Persistent Lactic Acidosis - Think beyond Sepsis Emily Pallister1* and Thogulava Kannan2 1 Check for ST5 Anaesthetics, University Hospitals of Coventry and Warwickshire, UK updates 2Consultant Anaesthetist, George Eliot Hospital, Nuneaton, UK *Corresponding author: Emily Pallister, ST5 Anaesthetics, University Hospitals of Coventry and Warwickshire, Coventry, UK Introduction • Differential diagnoses for hyperlactatemia beyond sepsis. A 79-year-old patient with type 2 diabetes mellitus was admitted to the Intensive Care Unit for manage- • Remember to check ketones in patients taking ment of Acute Kidney Injury refractory to fluid resusci- Metformin who present with renal impairment. tation. She had felt unwell for three days with poor oral • Recovery can be protracted despite haemofiltration. intake. Admission bloods showed severe lactic acidosis and Acute Kidney Injury (AKI). • Suspect digoxin toxicity in patients on warfarin with acute kidney injury, who develop cardiac manifes- The patient was initially managed with fluid resus- tations. citation in A&E, but there was no improvement in her acid/base balance or AKI. The Intensive Care team were Case Description asked to review the patient and she was subsequently The patient presented to the Emergency Depart- admitted to ICU for planned haemofiltration. ment with a 3 day history of feeling unwell with poor This case presented multiple complex concurrent oral intake. On examination, her heart rate was 48 with issues. Despite haemofiltration, acidosis persisted for blood pressure 139/32.
    [Show full text]
  • Unit 4 Acid-Base Homeostasis
    Vanderbilt University Medical Center Emergency General Surgery Service Surgical Residency Rotation and Curriculum UNIT 4 ACID-BASE HOMEOSTASIS UNIT OBJECTIVES: 1. Demonstrate an understanding of the biochemistry and physiology of acid-base homeostasis. 2. Demonstrate the ability to diagnose and effectively treat complex disorders of acid-base balance. COMPETENCY-BASED KNOWLEDGE OBJECTIVES: 1. Explain hydrogen ion biochemistry and physiology to include: a. The Henderson-Hasselbalch equation (1) Ventilatory component (pCO2) (2) Renal component (HCO3-) 2. Classify metabolic acidosis, including "anion gap" and hyperchloremic acidosis. 3. Identify specific causes of metabolic acidosis. 4. Given values for pH, pCO2, and HCO3-, distinguish between metabolic acidosis, respiratory acidosis, metabolic alkalosis, respiratory alkalosis, and mixed abnormalities; derive a differential diagnosis for each. 5. Predict the importance of primary diseases and their complications to the evaluation of patient risk for: a. Shock b. Bowel obstruction c. Sepsis 6. Analyze the acid-base problem and its cause in specific clinical situations, and determine an appropriate course of therapy for the following conditions: a. "Medical" problems such as: (1) Diabetic ketoacidosis (2) Lactic acidosis (3) Renal tubular acidosis (4) Renal insufficiency (5) Respiratory failure b. "Surgical" problems such as: (1) Gastric outlet obstruction (2) Fistulas (3) Shock COMPETENCY-BASED PERFORMANCE OBJECTIVES: 1. Diagnose and treat acid-base disturbances of all types. 2. Diagnose and treat complex and combined problems in acid-base disturbances as a component of overall care. 3. Manage complex situations in the intensive care unit where acid-base Vanderbilt University Medical Center Emergency General Surgery Service Surgical Residency Rotation and Curriculum abnormalities coexist with other metabolic derangements, including: a.
    [Show full text]
  • Lecture-1 Keto Acidosis, Bovine Ketosis, Ovine Pregnancy Toxemia
    Lecture-1 Keto acidosis Ketoacidosis is a metabolic acidosis due to an excessive blood concentration of ketone bodies (acetone, acetoacetate and beta-hydroxybutyrate). Ketone bodies are released into the blood from the liver when hepatic lipid metabolism has changed to a state of increased ketogenesis. The abnormal accumulation of ketones in the body occurs due to excessive breakdown of fats in deficiency or inadequate use of carbohydrates. It is characterized by ketonuria, loss of potassium in the urine, and a fruity odor of acetone on the breath. Untreated, ketosis may progress to ketoacidosis, coma, and death. This condition is seen in starvation, occasionally in pregnancy if the intake of protein and carbohydrates is inadequate, and most frequently in diabetes mellitus. Different Types of Ketoacidosis Diabetes Keto Acidosis (DKA): Due to lack of insulin glucose uptake and metabolism by cells is decrased.Fatty acid catabolism increased in resulting in excess production of ketone bodies. Starvation Ketosis: Starvation leads to hypoglycemia as there is little or no absorption of glucose from intestine and also due to depletion of liver glycogen. In Fatty acid oxidation leads to excess ketone body. Bovine Ketosis Introduction Bovine ketosis occurs in the high producing dairy cows during the early stages of lactation, when the milk production is generally the highest. Abnormally high levels of the ketone bodies, acetone, acetoacetic and beta-hydroxy butyric acid and also iso- propanol appear in blood, urine and in milk. The alterations are accompanied by loss of appetite , weight loss, decrease in milk production and nervous disturbances. Hypoglycemia (starvation) is a common finding in bovine ketosis and in ovine pregnancy toxemia.
    [Show full text]
  • Diabetic Ketoalkalosis in Children and Adults
    Original Article Diabetic Ketoalkalosis in Children and Adults Emily A. Huggins, MD, Shawn A. Chillag, MD, Ali A. Rizvi, MD, Robert R. Moran, PhD, and Martin W. Durkin, MD, MPH and DR are calculated because the pH and bicarbonate may be near Objectives: Diabetic ketoacidosis (DKA) with metabolic alkalosis normal or even elevated. In addition to having interesting biochemical (diabetic ketoalkalosis [DKALK]) in adults has been described in the features as a complex acid-base disorder, DKALK can pose diagnostic literature, but not in the pediatric population. The discordance in the and/or therapeutic challenges. change in the anion gap (AG) and the bicarbonate is depicted by an Key Words: delta ratio, diabetic ketoacidosis, diabetic ketoalkalosis, elevated delta ratio (DR; rise in AG/drop in bicarbonate), which is metabolic alkalosis normally approximately 1. The primary aim of this study was to de- termine whether DKALK occurs in the pediatric population, as has been seen previously in the adult population. The secondary aim was iabetic ketoacidosis (DKA), a common and serious dis- to determine the factors that may be associated with DKALK. Dorder that almost always results in hospitalization, is de- Methods: A retrospective analysis of adult and pediatric cases with a fined by the presence of hyperglycemia, reduced pH, metabolic 1 primary or secondary discharge diagnosis of DKA between May 2008 and acidosis, elevated anion gap (AG), and serum or urine ketones. August 2010 at a large urban hospital was performed. DKALK was as- In some situations, a metabolic alkalosis coexists with DKA sumedtobepresentiftheDRwas91.2 or in cases of elevated bicarbonate.
    [Show full text]
  • Diabetic Ketoacidosis: Evaluation and Treatment DYANNE P
    Diabetic Ketoacidosis: Evaluation and Treatment DYANNE P. WESTERBERG, DO, Cooper Medical School of Rowan University, Camden, New Jersey Diabetic ketoacidosis is characterized by a serum glucose level greater than 250 mg per dL, a pH less than 7.3, a serum bicarbonate level less than 18 mEq per L, an elevated serum ketone level, and dehydration. Insulin deficiency is the main precipitating factor. Diabetic ketoacidosis can occur in persons of all ages, with 14 percent of cases occurring in persons older than 70 years, 23 percent in persons 51 to 70 years of age, 27 percent in persons 30 to 50 years of age, and 36 percent in persons younger than 30 years. The case fatality rate is 1 to 5 percent. About one-third of all cases are in persons without a history of diabetes mellitus. Common symptoms include polyuria with polydipsia (98 percent), weight loss (81 percent), fatigue (62 percent), dyspnea (57 percent), vomiting (46 percent), preceding febrile illness (40 percent), abdominal pain (32 percent), and polyphagia (23 percent). Measurement of A1C, blood urea nitro- gen, creatinine, serum glucose, electrolytes, pH, and serum ketones; complete blood count; urinalysis; electrocar- diography; and calculation of anion gap and osmolar gap can differentiate diabetic ketoacidosis from hyperosmolar hyperglycemic state, gastroenteritis, starvation ketosis, and other metabolic syndromes, and can assist in diagnosing comorbid conditions. Appropriate treatment includes administering intravenous fluids and insulin, and monitoring glucose and electrolyte levels. Cerebral edema is a rare but severe complication that occurs predominantly in chil- dren. Physicians should recognize the signs of diabetic ketoacidosis for prompt diagnosis, and identify early symp- toms to prevent it.
    [Show full text]
  • Diabetic Ketoacidosis Diabetic Ketoacidosis (DKA) Is a Serious Problem That Can Happen in People with Diabetes
    Diabetic Ketoacidosis Diabetic ketoacidosis (DKA) is a serious problem that can happen in people with diabetes. DKA should be treated as a medical emergency. This is because it can lead to coma or death. If you have the symptoms of DKA, get medical help right away. DKA happens more often in people with type 1 diabetes. But it can happen in people with type 2 diabetes. It can also happen in women with diabetes during pregnancy (gestational diabetes). DKA happens when insulin levels are too low. Without enough insulin, sugar (glucose) can’t get to the cells of your body. The glucose stays in the blood. The liver then puts out even more glucose into the blood. This causes high blood glucose (hyperglycemia). Without glucose, your body breaks down stored fat for energy. When this happens, acids called ketones are released into the blood. This is called ketosis. High levels of ketones (ketoacidosis) can be harmful to you. Hyperglycemia and ketoacidosis can also cause serious problems in the blood and your body, such as: • Low levels of potassium (hypokalemia) and phosphate • Damage to kidneys or other organs • Coma What causes diabetic ketoacidosis? In people with diabetes, DKA is most often caused by too little insulin in the body. It is also caused by: • Poor management of diabetes • Infections such as a urinary tract infection or pneumonia • Serious health problems, such as a heart attack • Reactions to certain prescribed medicines including SGLT2 inhibitors for treating type 2 diabetes • Reactions to illegal drugs including cocaine • Disruption of insulin delivery from an insulin pump Symptoms of diabetic ketoacidosis DKA most often happens slowly over time.
    [Show full text]
  • Observations Compensatory Hypochloraemic Alkalosis In
    Letters 871 tended to the DQ-LTR13 integration, where we also find a con- 2. Pascual M, Martin J, Nieto A et al. (2001) Distribution of tribution of DQ-LTR13 to RA susceptibility in DQ8-positive HERV-LTR elements in the 5′-flanking region of HLA- individuals. Furthermore we recently published that patients DQB1 and association with autoimmunity. Immunogenetics with Addison’s disease—another HLA DQ8-associated autoim- 53:114–118 mune disease of the adrenals which may occur in combination 3. Donner H, Tonjes RR, Bontrop RE et al. (1999) Intronic se- with Type 1 diabetes as part of the autoimmune pluriglandular quence motifs of HLA-DQB1 are shared between humans, syndrome Type 2—have more often the DQ8-DQ-LTR13 com- apes and Old World monkeys, but a retroviral LTR element bination in contrast to the DQ-LTR3 insertion. Although both (DQLTR3) is human specific. Tissue Antigens 53:551–558 DQ-LTR3 and DQ-LTR13 are linked to DQ8, DQ-LTR13 en- 4. Donner H, Tonjes RR, Van der Auwera B et al. (1999) The hances the risk for Addison’s disease [7]. presence or absence of a retroviral long terminal repeat Whether DQ-LTR13 has a functional significance or not is influences the genetic risk for type 1 diabetes conferred by currently under investigation. Preliminary data indicate that human leukocyte antigen DQ haplotypes. J Clin Endocrinol DQ-LTR13 harbours regulatory capacity and shows functional Metab 84:1404–1408 activity of an upstream element as revealed by analyses of nu- 5. Seidl C, Donner H, Petershofen E et al.
    [Show full text]
  • Hypertension Despite Dehydration in an Adolescent with Diabetic Ketoacidosis
    CASE REPORT Hypertension Despite Dehydration in an Adolescent with Diabetic Ketoacidosis Alphonsus N. Onyiriuka, Promise Monday, Chinwe A. Oguejiofor Endocrine and Metabolic Unit, Department of Child Health, University of Benin Teaching Hospital, Benin City, Nigeria. Corresponding Author: Alphonsus N. Onyiriuka, MD. Endocrine and Metabolic Unit, Department of Child Health, University of Benin Teaching Hospital, PMB 1111, Benin City, Nigeria. email: [email protected]. ABSTRAK Secara umum, informasi mengenai perubahan tekanan darah pada ketoasidosis diabetik remaja sangat langka. Tujuan artikel ini melaporkan kasus DKA parah pada seorang gadis remaja yang secara tak terduga mengalami hipertensi dari sebelumnya hipotensi. Kasus seorang gadis berusia 17 tahun di unit gawat darurat anak dengan keluhan makan berlebihan selama 6 minggu, buang air kecil yang berlebihan selama 2 minggu, demam selama 1 minggu, muntah selama 4 hari, kesulitan bernafas selama satu hari dan tidak responsif menelepon selama 3 jam. Dia telah mengalami dehidrasi berat namun tidak mengalami hipotensi. Temuan laboratorium termasuk hiperglikemia (glukosa darah sewaktu 20,8 mmol/L; 347 mg/dl), asidosis (serum bikarbonat 5 mmol/L), ketonuria 2+; glikosuria 2+, dan berat jenis urine 1.015. Saat masuk, tekanan darah 100/60 mmHg tetapi semakin meningkat menjadi 140- 180/80-100 mmHg pada hari ketiga saat masuk. Hipertensi yang signifikan dapat terjadi pada anak-anak dan remaja yang dirawat karena DKA parah meskipun ada dehidrasi. Oleh karena itu, dokter yang hadir harus waspada terhadap kemungkinan ini. Key words: ketoasidosis diabetik, dehidrasi, hipertensi. ABSTRACT In general, information on blood pressure changes in diabetic ketoacidosis in paediatric population is very scarce. Our aim was to report a case of severe DKA in an adolescent girl who unexpectedly had hypertension rather than hypotension.
    [Show full text]
  • ACS/ASE Medical Student Core Curriculum Acid-Base Balance
    ACS/ASE Medical Student Core Curriculum Acid-Base Balance ACID-BASE BALANCE Epidemiology/Pathophysiology Understanding the physiology of acid-base homeostasis is important to the surgeon. The two acid-base buffer systems in the human body are the metabolic system (kidneys) and the respiratory system (lungs). The simultaneous equilibrium reactions that take place to maintain normal acid-base balance are: H" HCO* ↔ H CO ↔ H O l CO g To classify the type of disturbance, a blood gas (preferably arterial) and basic metabolic panel must be obtained. A basic understanding of normal acid-base buffer physiology is required to understand alterations in these labs. The normal pH of human blood is 7.40 (7.35-7.45). This number is tightly regulated by the two buffer systems mentioned above. The lungs contain carbonic anhydrase which is capable of converting carbonic acid to water and CO2. The respiratory response results in an alteration to ventilation which allows acid to be retained or expelled as CO2. Therefore, bradypnea will result in respiratory acidosis while tachypnea will result in respiratory alkalosis. The respiratory buffer system is fast acting, resulting in respiratory compensation within 30 minutes and taking approximately 12 to 24 hours to reach equilibrium. The renal metabolic response results in alterations in bicarbonate excretion. This system is more time consuming and can typically takes at least three to five days to reach equilibrium. Five primary classifications of acid-base imbalance: • Metabolic acidosis • Metabolic alkalosis • Respiratory acidosis • Respiratory alkalosis • Mixed acid-base disturbance It is important to remember that more than one of the above processes can be present in a patient at any given time.
    [Show full text]
  • Ketogenesis & Ketone Bodies
    THE METABOLISM OF KETONE BODIES KETOGENESIS CLINICAL SIGNIFICANCE OF KETOGENESIS • The production of ketone bodies occurs at a relatively low rate during normal feeding and under conditions of normal physiological status. • Normal physiological responses to carbohydrate shortages cause the liver to increase the production of ketone bodies from the acetyl-CoA generated from fatty acid oxidation. This allows the heart and skeletal muscles primarily to use ketone bodies for energy, thereby preserving the limited glucose for use by the brain. • The most significant disruption in the level of ketosis, leading to profound clinical manifestations, occurs in untreated insulin- dependent diabetes mellitus. This physiological state, diabetic ketoacidosis (DKA), results from a reduced supply of glucose (due to a significant decline in circulating insulin) and a concomitant increase in fatty acid oxidation (due to a concomitant increase in circulating glucagon). • The increased production of acetyl-CoA leads to ketone body production that exceeds the ability of peripheral tissues to oxidize them. • Ketone bodies are relatively strong acids (pKa around 3.5), and their increase lowers the pH of the blood. This acidification of the blood is dangerous chiefly because it impairs the ability of hemoglobin to bind oxygen. • It is important to note that animals are unable to convert fatty acids into glucose. • Specifically, acetyl CoA cannot be converted into pyruvate or oxaloacetate in animals. • The two carbon atoms of the acetyl group of acetyl CoA enter the citric acid cycle, but two carbon atoms leave the cycle in the decarboxylations catalyzed by isocitrate dehydrogenase and a-ketoglutarate dehydrogenase. • Consequently, oxaloacetate is regenerated but it is not formed de novo when the acetyl unit of acetyl CoA is oxidized by the citric acid cycle.
    [Show full text]
  • The Accuracy of Clinical Assessment of Dehydration During Diabetic Ketoacidosis in Childhood
    BRIEF REPORT The Accuracy of Clinical Assessment of Dehydration During Diabetic Ketoacidosis in Childhood 1 1 ILDIKO H. KOVES, MD GEORGE A. WERTHER, MD hydration categories as those used for the 2 2 JOCELYN NEUTZE, MD PETER BARNETT, MD doctors’ assessments. 3 1 SUSAN DONATH, MA FERGUS J. CAMERON, MD 1 WARREN LEE, MD Statistical analysis Agreement between the doctor’s assess- ments of dehydration and between as- sessed and measured dehydration were Ͻ he objective of this study was to ex- were pH 7.30 (capillary, venous, or ar- evaluated using ␬-statistics (5). amine the accuracy of the assess- terial) and/or bicarbonate Ͻ15 mmol/l T ment of clinical dehydration in and ketones in the urine on dipstick test- children with type 1 diabetes and diabetic ing. The following information was re- RESULTS — The greatest number of ketoacidosis (DKA). DKA remains the sin- corded by the primary assessing doctor: patients (18 of 37) were between 5 and gle most common cause of diabetes- newly diagnosed or established diabetes, 10% dehydrated at presentation (as related death in childhood (1). Accurate age, sex, date and time seen, heart rate, calculated by their weight gains), with assessment and management of dehydra- respiratory rate, blood pressure, pale a median absolute measure of 8.7% tion is the cornerstone of DKA treatment and/or cool hands and feet, peripheral dehydration. (1,2). The assessment of the degree of capillary refill time, reduced skin turgor, There was a good level of agreement dehydration has traditionally been ac- level of consciousness (on a rating scale of between the primary and secondary as- cording to clinical criteria including pe- one to eight), sunken eyes, sunken fonta- sessor (␬ϭ0.5).
    [Show full text]