Diabetic ketoacidosis in children pdf

No response 1. No motor response 2. Eyes open to pain 2. No words, only 2. Inconsolable, irritable, 2. Extension to pain incomprehensible sounds; restless, cries decerebrate posture moaning 3. Eyes open to verbal 3. Inconsistently consolable 3. Flexion to pain decorticate command and moans; makes vocal posture sounds 4. Eyes open 4. Confused, disoriented 4. Consolable when crying and 4.

Orientated, normal 5. Smiles, oriented to sound, 5. Localizes pain conversation follows objects and interacts 6. Supportive measures consciousness or those who are at increased risk for cerebral edema e. An arterial catheter may be necessary in In a child with established diabetes, whose parents some critically ill patients managed in an intensive have been trained in sick day management, hyper- care unit.

There should be documentation on a flow chart Where should the child be managed? Increased o rising blood pressure serum urea nitrogen and hematocrit may be useful o decreased oxygen saturation markers of the severity of ECF contraction 44, The latter is not curate in the presence of poor peripheral circulation a concern with most modern methods for measuring and acidosis. As the hematocrit, and blood gases should be repeated 2- plasma glucose concentration decreases after adminis- hourly for the first 12 hours, or more frequently, as tering fluid and insulin, the measured serum sodium clinically indicated, in more severe cases.

A failure of measured serum sodium 2 hours 38, Clinical estimates of the volume facility before assessment should be factored into deficit are subjective and inaccurate 53, 54 ; therefore, calculation of deficit and repair E.

See Tables 1 and 3 for 28 examples of calculations. Table 3 gives volumes for maintenance and rehydration per 24 hours and per hour. If fluid has been given for Insulin therapy resuscitation, the volume should not be subtracted from the amount shown in the table.

Fluids given orally when DKA is caused by a decrease in effective circulating patient has improved should be subtracted from the amount insulin associated with increases in counter-regulatory in the table. Table 3 is based on maintenance volumes hormones glucagon, catecholamines, GH, cortisol. Intracellular potassium is depleted because of the anion gap , which invariably takes longer than transcellular shifts of this ion caused by hypertonicity normalization of blood glucose concentrations B increased plasma osmolality causes solvent drag Potassium is lost from the body from vomiting established diabetes , the dose may be decreased to and as a consequence of osmotic diuresis.

Volume 0. Thereafter, serum potassium levels may be normal, increased and after commencing insulin therapy, the plasma or decreased Administration of amount of glucose administration C 79— The serum potassium concentration may should be added to the IV fluid e. Tall, peaked, symmetrical, T waves tion is not possible, hourly or 2-hourly SC or IM and shortening of the QT interval are signs of hyper- administration of a short- or rapid-acting insulin kalemia.

Subsequent potas- C 80, 86—89 , but should not be used in subjects sium replacement therapy should be based on serum whose peripheral circulation is impaired E. Total body phosphate depletion has been associated with a variety of metabolic disturbances 97— Clinically Introduction of oral fluids and transition to SC significant hypophosphatemia may occur if intravenous insulin injections therapy without food intake is prolonged beyond 24 hours 45— With intermediate- or long-acting insulin, the over- Acidosis lap should be longer and the IV insulin gradually Severe acidosis is reversible by fluid and insulin lowered.

For example, for patients on a basal-bolus replacement; insulin stops further ketoacid production insulin regimen, the first dose of basal insulin may be and allows ketoacids to be metabolized, which administered in the evening and the insulin infusion generates bicarbonate A. Treatment of hypovolemia is stopped the next morning E. In national population studies, the mortality rate from Nevertheless, there may be selected patients who may DKA in children is 0.

The pathogenesis of both before treatment has begun 60, , — or, its initiation and progression is unclear and incom- rarely, may develop as late as 24—48 hours after the pletely understood. Demographic factors that have start of treatment C,B 60, , Symptoms and been associated with an increased risk of cerebral edema signs are variable.

Blood rate rarely in excess of 1. Pediatrics 1 : 84— Do Diabetic ketoacidosis: a potassium. Diabetes Care Aug: 23 8 : —4. Incidence and onset features of diabetes in African- American and Latino children in Chicago, — Diabet Med Oct: 21 10 : —8. Screening for tol should be given immediately.

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Hyperglycemic crises in adult patients mellitus in Japan Clin Pediatr Endocrinol 14 2 : with diabetes: a consensus statement from the American 65— Diabetes Association.

Diabetes Care Dec: 29 12 : Diabetic ketoaci- — A 2-yr national Pediatr Rev Apr: 11 10 : — Death caused by predisposing conditions and insulin pump use.

Pediatr hyperglycemic hyperosmolar state at the onset of type Diabetes Feb: 10 1 : 33—7. J Pediatr Feb: 2 : —3. Childhood diabetes presenting with dosis, hyperosmolarity and hypernatremia: are high- hyperosmolar dehydration but without ketoacidosis: carbohydrate drinks worsening initial presentation? Decompensated hyper- consensus statement on diabetic ketoacidosis in children glycemic hyperosmolarity without significant ketoaci- and adolescents.

Arch Dis Child Feb: 89 2 : dosis in the adolescent and young adult population. J — Pediatr Endocrinol Metab Oct: 20 10 : — Short-term Hyperglycemic crises fasting is a mechanism for the development of in diabetes mellitus: diabetic ketoacidosis and hyper- euglycemic ketoacidosis during periods of insulin glycemic hyperosmolar state.

Endocrinol Metab Clin deficiency. Presentation and progress of childhood and laboratory features of type 1 diabetic children at diabetes mellitus: a prospective population-based study.

Diabetologia — American Diabetes Association. Ketoacidosis at the diagnosis of type in children and adolescents. Consensus statement. Childhood Diabetes 9. Diabetic in Finland Study Group. Arch Dis Child 75 5 : ketoacidosis among obese African-American adoles- —5. Diabetes Care 20 4 : —6. European and Dibetes. Diabetologia Oct: management of diabetic ketoacidosis in children.

Dia- 44 Suppl 3 : B75— Diabetic The value of electrocar- ketoacidosis and cerebral oedema in Sweden—a 2-year diogram monitoring in diabetic ketoacidosis. Diabetes paediatric population study. Diabetes Jul: Ethnicity and young age influence the frequency of 23 7 : —5.

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Trans Assoc Am Physicians —9. A cross-sectional Studies in diabetic acidosis and 1 diabetes. The French Pediatric Diabetes Group [see coma, with particular emphasis on the retention of comments]. Diabetes Care 21 7 : — J Clin Invest 1—9. Ketoacidosis occurring in newly diag- electrolyte during recovery in a patient with diabetic nosed and established diabetic children.

Acta Paediatr acidosis. J Pediatr — The maintenance need for Adherence 19 5 : — Pediatric hydration therapy: historical dosis in insulin-dependent diabetes mellitus. The review and a new approach. Diabetes Audit and —8. A month-old was added to the few reported pediatric cases in This acute, rapidly progressing, and often fatal facultative fungal infection occurs in young patients with diabetes who have chronically poor glycemic control and ketoacidosis.

The principal locus may be rhinocerebral, pulmonary, cutaneous, gastrointestinal, or in the CNS, or it may be disseminated. In a series of five patients, the sole survivor had severe neurologic disability; risk factors were African American race and history of poor compliance poor clinic attendance, risk-taking behaviors, and high rate of hospital admission.

In , two teenage patients were reported with fatal CE and only three others were identified from the literature with a similar clinical history. These reports have provided incidence data and have emphasized the idiosyncratic nature of the occurrence of CE and the absence of iatrogenic causation. A 3-year United Kingdom population-based study yielded an incidence of 0. Earlier reports may reflect biased fatality and residual morbidity data and later recognition than more recent population-based observations.

Appropriate intervention was also less frequent in these earlier-reported and litigated cases. This may reflect the more rapid deterioration in this age group and greater delay in diagnosis because of nonspecificity of symptoms. The younger brain might also be more susceptible to metabolic and vascular changes associated with DKA. Severity of acidosis, degree of hypocapnia, and elevated serum urea nitrogen, indicators of severity of ketoacidosis and dehydration, have been noted to be risk factors.

CE associated with DKA is rarely seen beyond the pediatric age group 0—21 years 67 or in adult patients with HHS, despite rapid rehydration and restoration of normal glycemia. This may be because those who are in the early, presymptomatic stages of CE experience changes in the brain that result in dysregulation of antidiuretic hormone secretion.

In the 61 children with CE from a North American multicenter study, worse outcomes occurred in those with greater neurologic depression at the time of diagnosis of CE and with higher initial serum urea nitrogen concentrations. CE refers to an increase of cerebral tissue water causing an increase of tissue volume. Neither the cause nor the location of the fluid in the swollen brains of children with DKA is known. The mechanism is likely to be complex, and it may not be the same in all affected individuals, as reflected by the time of onset and the brain imaging findings.

The time of onset is distributed in a bimodal fashion, with approximately two-thirds of patients developing signs and symptoms in the first 6—7 hours and the rest from 10—24 hours after the start of treatment, with the early-onset individuals tending to be younger. Twenty-six percent had diffuse edema, which was also similar between early and late onset. These localized injuries were only in the early-onset patients. Because treatment modification has not prevented CE and with the strong evidence that early administration of mannitol prevents brain damage and death from this complication, Muir et al.

This means that five youngsters will be treated for CE to prevent brain damage or death in one patient, a reasonable proposition considering the alternative of waiting for more stringent criteria to be met. Improvement has been consistently observed with administration of IV mannitol in a dosage of 1.

Although early intervention with mannitol treatment has improved outcome, it is difficult to determine to what degree, because increased recognition of the problem has undoubtedly led to less stringent case definition. The application of criteria developed by Muir et al. Mannitol lowers the hematocrit and blood viscosity, improving cerebral blood flow CBF and oxygenation, red cell deformability, and vasoconstriction in areas of the brain with intact autoregulation.

It may also improve autoregulation from the effects on CBF and oxygenation, and has direct osmotic effects with reduction in extracellular free water. Intensivists frequently express concern about the use of mannitol because of their experience with the risk of rebound edema and renal failure when mannitol is used over an extended period. However, there are no reports of complications of mannitol use in this acute situation.

Hypertonic saline HS has become the standard for treating acute intracranial hypertension in head injury and following surgical procedures in the supratentorial region and in these circumstances has been considered at least as effective as mannitol. Intubation should be reserved for those with respiratory compromise, but should not be undertaken simply because of the diagnosis of CE.

Aggressive hyperventilation was a significant risk factor for poor outcome in the study of Marcin et al. Prevention of DKA at onset is most dramatically demonstrated when early diagnosis is made through genetic and immunologic screening of high-risk children. In the s, a comprehensive approach involving outreach clinics, frequent routine and emergency telephone contact, and a camping program supported by state funding for children with special healthcare needs dramatically reduced recurrent DKA episodes.

Private patients in the program had a reduction in hospital admission days from preintervention of 2. The children sponsored by the state program had a reduction from 4. Patients with compliance problems account for a disproportionate number of recurrent DKA episodes. In the UK surveillance study, 4. DKA is the result of absolute or relative deficiency of insulin in combination with exuberant secretion of counter-regulatory hormones glucagon, catecholamines, cortisol, growth hormone resulting in blockade of glucose utilization in insulin-sensitive tissues liver, fat, muscle and a cascade of derangement progressing to ketoacidosis and dehydration.

Much new-onset DKA can be prevented by increased awareness of early signs and symptoms of diabetes and, in principle, almost all recurrent DKA is preventable by informed sick day management, recognition of psychosocial problems leading to insulin omission, and careful monitoring of insulin pump function.

Management of DKA should occur in centers with treatment experience and monitoring capability. Fluid replacement begins with 0. Whether levels of serum K are normal or elevated, there will be a total K deficit that must be dealt with early and sufficiently. Bicarbonate administration is neither necessary nor safe. Mannitol or hypertonic saline should be at the bedside, for rapid intervention as indicated for CE, the most common serious complication of DKA.

Other complications include hypokalemia, hypophosphatemia, hypoglycemia, intracerebral complications other than CE, peripheral venous thrombosis, mucormycosis, aspiration pneumonia, rhabdomyolysis, acute pancreatitis, and acute renal failure. Among questions that need to be addressed regarding DKA in children and adolescents are whether feasible and cost-effective methods can reduce the frequency of new-onset and recurrent DKA, what characterizes optimal fluid replacement therapy, how effective proposed monitoring and intervention criteria are in the reduction of CE morbidity and mortality, and whether hypertonic saline is as or more effective than mannitol in the treatment of CE.

Treatment of DKA requires first and foremost fluid resuscitation with 0. Insulin should not be given as a bolus, but infused after the initial fluid resuscitation in a dose of 0. CE is the most common serious complication, requiring careful neurologic and vital sign monitoring and early intervention with mannitol or hypertonic saline infusion. The author has no conflicts of interest to declare.

Open Access. This article is distributed under the terms of the Creative Commons Attribution Noncommercial License which permits any noncommercial use, distribution, and reproduction in any medium, provided the original author s and source are credited. This article is published with open access at Springerlink. National Center for Biotechnology Information , U.

Journal List Diabetes Ther v. Diabetes Ther. Published online Jan Arlan L. Rosenbloom 1, 2. Author information Article notes Copyright and License information Disclaimer. Rosenbloom, Email: ude.

Corresponding author. Received Oct This article has been cited by other articles in PMC. Abstract The object of this review is to provide the definitions, frequency, risk factors, pathophysiology, diagnostic considerations, and management recommendations for diabetic ketoacidosis DKA in children and adolescents, and to convey current knowledge of the causes of permanent disability or mortality from complications of DKA or its management, particularly the most common complication, cerebral edema CE.

Keywords: adolescents, cerebral edema, children, complications, diabetic ketoacidosis, fluid replacement, hypokalemia, management, prevention, recurrent DKA.

Pathophysiology DKA is the result of a critical relative or absolute deficit of insulin, resulting in intracellular starvation of insulin-dependent tissues muscle, liver, adipose , stimulating the release of the counter-regulatory hormones glucagon, catecholamines, cortisol, and growth hormone. Open in a separate window. Frequency and Risk Factors DKA with New-Onset Diabetes The frequency of new-onset diabetes presenting as DKA varies widely by geographic region, and correlates inversely with the regional incidence, and therefore the level of awareness in the community of pediatric diabetes.

Best eye response Best verbal response Best verbal response nonverbal children Best motor response 1. No eye opening 1. No verbal response 1. No response 1. No motor response 2. Eyes open to pain 2. No words, only incomprehensible sounds; moaning and groaning 2.

Inconsolable, irritable, restless, cries 2. Extension to pain decerebrate posture 3. Eyes open to verbal command 3. Inconsistently consolable and moans; makes vocal sounds 3.

Flexion to pain decorticate posture 4. Eyes open spontaneously 4. Consolable when crying and interacts inappropriately 4. Withdrawal from pain 5. Orientated, normal conversation 5.

Smiles, oriented to sound, follows objects and interacts 5. Localizes pain 6. Obeys commands. Management Children with established diabetes, who are not vomiting or severely ill, and whose caregiver has been trained in sick day management, can be managed at home or at an outpatient facility, with appropriate supervision and follow-up.

Replace electrolyte losses. Intervene rapidly when complications, especially CE, occur. Insulin Insulin should be started after initial fluid expansion.

Monitoring Successful management and early intervention for complications requires close monitoring. Transition IV fluids can be stopped 1—2 hours after substantial consumption of oral fluids without vomiting. Established patients with DKA can resume their usual home dose of insulin. Rhabdomyolysis Rhabdomyolysis is a common complication of HHS and is associated with renal failure.

Mucormycosis This acute, rapidly progressing, and often fatal facultative fungal infection occurs in young patients with diabetes who have chronically poor glycemic control and ketoacidosis. Cerebral Edema In , two teenage patients were reported with fatal CE and only three others were identified from the literature with a similar clinical history.

Morbidity and Mortality Earlier reports may reflect biased fatality and residual morbidity data and later recognition than more recent population-based observations. Mechanisms CE refers to an increase of cerebral tissue water causing an increase of tissue volume.

Monitoring Because treatment modification has not prevented CE and with the strong evidence that early administration of mannitol prevents brain damage and death from this complication, Muir et al. Treatment Improvement has been consistently observed with administration of IV mannitol in a dosage of 1.

Prevention of DKA Prevention of DKA at onset is most dramatically demonstrated when early diagnosis is made through genetic and immunologic screening of high-risk children. Conclusion DKA is the result of absolute or relative deficiency of insulin in combination with exuberant secretion of counter-regulatory hormones glucagon, catecholamines, cortisol, growth hormone resulting in blockade of glucose utilization in insulin-sensitive tissues liver, fat, muscle and a cascade of derangement progressing to ketoacidosis and dehydration.

Key points Treatment of DKA requires first and foremost fluid resuscitation with 0. Bicarbonate infusion is contraindicated in pediatric DKA. Acknowledgments The author has no conflicts of interest to declare. Footnotes This article is published with open access at Springerlink. References 1. American Diabetes Association. Position statement: hyperglycemic crises in patients with diabetes mellitus. Diabetes Care. Wolfsdorf J. Diabetic ketoacidosis in children and adolescents with diabetes.

Pediatr Diabetes. Burge M. Short-term fasting is a mechanism for the development of euglycemic ketoacidosis during periods of insulin deficiency. J Clin Endocrinol Metab. Pinkey J. Presentation and progress of childhood diabetes mellitus: a prospective population-based study. Kitabchi A. Hyperglycemic crises in adult patients with diabetes.

Foster D. The metabolic derangements and treatment of diabetic ketoacidosis. N Engl J Med. Bui T. Trends in diabetic ketoacidosis in childhood and adolescence: a yr experience. Jackson W. The changing presentation of children with newly diagnosed type 1 diabetes mellitus. In infants, toddlers, and preschool-age children, some clinicians use relatively smaller proportions of rapid-acting insulin before breakfast and dinner e. TDD, total daily dose.

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Management of DKA. Article Navigation. This Site. Google Scholar. Mark A. Sperling, MD Mark A. Sperling, MD. Address correspondence and reprint requests to Dr. Diabetes Care ;29 5 — Get Permissions. Look for acanthosis nigricans suggesting insulin resistance and type 2 diabetes. Perform a urinalysis for ketones. Give oxygen to patients with severe circulatory impairment or shock. Give antibiotics to febrile patients after obtaining appropriate cultures of body fluids.

The child should receive care in a unit that has: Experienced nursing staff trained in monitoring and management Written guidelines for DKA management in children Access to laboratories for frequent and timely evaluation of biochemical variables A specialist with training and expertise in the management of DKA should direct inpatient management.

Amount of administered insulin. Urine ketones until cleared. Figure 1—. View large Download slide. Table 1— Symptoms and signs of cerebral edema. Headache Recurrence of vomiting Inappropriate slowing of heart rate Rising blood pressure Decreased oxygen saturation Change in neurological status: Restlessness, irritability, increased drowsiness, incontinence Specific neurologic signs, e. View Large. Table 2— Usual losses of fluids and electrolytes in DKA and normal maintenance requirements.

Average losses per kg range. Maintenance requirements. Fluid and electrolyte. Approximate requirements for maintenance 48 h. Working total 48 h. Approximate duration and rate. Fluid composition and volume. Sodium mEq. Potassium mEq. Chloride mEq. Phosphate mmol. Table 5— Insulin regimens for newly diagnosed diabetes after resolution of DKA. Prepubertal TDD 0. Diabet Med. Arch Dis Child. Pediatr Diabetes. N Engl J Med. J Pediatr. Diabetes Care.

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Arch Pediatr Adolesc Med. Katz MA: Hyperglycemia-induced hyponatremia: calculation of expected serum sodium depression. Am J Med. Adrogue HJ, Barrero J, Eknoyan G: Salutary effects of modest fluid replacement in the treatment of adults with diabetic ketoacidosis: use in patients without extreme volume deficit.

Kitabchi AE: Low-dose insulin therapy in diabetic ketoacidosis: fact or fiction? Diabetes Metab Rev. J Clin Endocrinol Metab. Lindsay R, Bolte RG: The use of an insulin bolus in low-dose insulin infusion for pediatric diabetic ketoacidosis. Ann Intern Med. Trans Assoc Am Physicians. Darrow D, Pratt E: Retention of water and electrolyte during recovery in a patient with diabetic acidosis. Medicine Baltimore. Am J Physiol. Guest G: Organic phosphates of the blood and mineral metabolism in diabetic acidosis.

Guest G, Rapoport S: Electrolytes of blood plasma and cells in diabetic acidosis and during recovery. Proc Am Diabetes Assoc. Knochel JP: The pathophysiology and clinical characteristics of severe hypophosphatemia. Arch Intern Med. Keller U, Berger W: Prevention of hypophosphatemia by phosphate infusion during treatment of diabetic ketoacidosis and hyperosmolar coma.

Clerbaux T, Reynaert M, Willems E, Frans A: Effect of phosphate on oxygen-hemoglobin affinity, diphosphoglycerate and blood gases during recovery from diabetic ketoacidosis. Intensive Care Med. Bohannon NJ: Large phosphate shifts with treatment for hyperglycemia. Ann Emerg Med. Edge JA: Cerebral oedema during treatment of diabetic ketoacidosis: are we any nearer finding a cause? Diabetes Metab Res Rev.