**8. Preventıon**

the mediastinum. Extension into neck and subcutaneous tissue could be seen. The most common sypmtoms include chest pain and dyspnoea. Treatment is mostly supportive; management of nausea/vomiting along with correction of acidosis to break Kussmaul breathing is should be considered. Patients should be carefully monitored in intensive

Symptomatic cerebral edema (CE) is rare in adults treated for DKA, although asympto‐ matic CE may be occur [224] and may be present before treatment [225]. In contrast to this, CE occurs in ~0.3–1.0% of DKA episodes in children [224,226) and is associated with a mortality rate of 20–40% [226] and accounts for 57–87% of all DKA deaths [224,226]. Because of possible delay in diagnosis and more susceptibility to metabolic and vascular changes, children <5 years of age have higher risk for the development of CE. The recog‐ nized risk factors for development of CE are acidosis, hypocapnia and elevated serum urea nitrogen (indicator of severity of ketoacidosis and dehydration) [227]. The etiology of CE is unknown; many mechanisms have been proposed including cerebral hypoperfu‐ sion with subsequent re-perfusion [228,229], the generation of various inflammatory me‐ diators [230], increased cerebral blood flow, disruption of cell membrane ion transport and a rapid shift in extracellular and intracellular fluids resulting in changes in osmolali‐ ty. Thus the etiology of DKA-related CE is multifactorial and results of an interplay of complex pathophysiological processes involving the brain [231-235]. The time of onset is not the same in all affected individuals; two-thirds of patients develops signs and symp‐ toms in the first 6-7 hours and the rest from 10-24 hours after start of the treatment with

Muir et al. suggested a model for early detection. The system allowed 92% sensitivity and 96% specificity for the recognition of CE early enough for intervention. One diagnostic crite‐ rion, two major criteria or one major plus two minor criteria is suitable to establish CE [236].

**Diagnostic criteria Major criteria Minor criteria**

1.Altered mentation and fluctuating

1.Vomiting following initial

at admission

than 90 mmHg 5. Age <5 years

sleep

treatment and its cessation, if present

3.Lethargy or not easily aroused from

4. Diastolic blood pressure greater

2. Headache (recurrent and more severe than on admission)

2.Sustained heart rate deceleration (decline more than 20 per minute) not attributable to improved intravascular volume or sleep state 3. Age inappropriate incontinence

the early-onset individuals tending to be younger [182,236,237].

**Table 6.** Diagnostic criteria, major criteria and minor criteria for Cerebral Edema

Diagnostic criteria, major criteria and minor criteria are shown in Table 6.

level of consciousness

care settings [221-223].

1. Abnormal motor or verbal

2.Decorticate or decerebrate posture 3.Cranial nerve palsy (especially III, IV,

4.Abnormal neurogenic respiratory

(eg: grunting, tachypnea, Cheyne-

response to pain

Stokes, apneustic)

VI)

pattern

**7.8. Cerebral edema**

272 Type 1 Diabetes

DKA can be prevented by access to a 24-hours telephone helpline for emergency advice and treatment, sufficient patient education and easier access to medical care. Especially patients should be educated about a clinical condition which increases the risk of developing DKA and the changes in the treatment at this situations.

These are includes the following;


Home measurement of blood glucose-ketone levels may allow early recognition of hyper‐ glycemia and ketosis. Adjusment of insulin therapy based on these findings may prevent hospitalization for DKA [246].

[7] Pinkney JH, Bingley PJ, Sawtell PA, et al. Presentation andb progress of childhood diabetes mellitus: a prospective population-based study. Diabetologia 1994;37:70-4. [8] White NH. Diabetic ketoacidosis in children. Endocrinol Metab Clin North Am. 2000

Diabetic Ketoacidosis

275

http://dx.doi.org/10.5772/53199

[9] Usher-Smith JA, Thompson MJ, Sharp SJ, Walter FM. Factors associated with the presence of diabetic ketoacidosis at diagnosis of diabetes in children and young

adults: a systematic review. BMJ. 2011 Jul 7;343:d4092. doi: 10.1136/bmj.d4092. [10] Kitabchi AE, Umpierrez GE, Murphy MB, Barrett EJ, Kreisberg RA, Malone JI, Wall BM. Management of hyperglycemic crises in patients with diabetes. Diabetes Care

[11] Komulainen J, Lounamaa R, Knip M, Kaprio EA, Akerblom HK. Ketoacidosis at the diagnosis of type 1 (insulin dependent) diabetes mellitus is related to poor residual beta cell function. Childhood Diabetes in Finland Study Group. Arch Dis Child. 1996

[12] DIAMOND Project Group. Incidence and trends of childhood type 1 diabetes world‐

[13] EURODIAB ACE Study Group. Variation and trends in incidence of childhood dia‐

[15] Patterson CC, Dahlquist GG, Gyürüs E, Green A, Soltész G; EURODIAB Study Group. Incidence trends for childhood type 1 diabetes in Europe during 1989-2003 and predicted new cases 2005-20: a multicentre prospective registration study. Lan‐

[16] Chiasson JL, Aris-Jilwan N, Belanger R, Bertrand S, Beauregard H, Ekoe JM, Fournier H, Havrankova J. Diagnosis and treatment of diabetic ketoacidosis and the hypergly‐

[17] Kitabchi AE, Nyenwe EA. Hyperglycemic crises in diabetes mellitus: diabetic ketoa‐ cidosis and hyperglycemic hyperosmolar state. Endocrinol Metab Clin North Am.

[18] Gurlek A, Erbas T, Sayinalp S, Gedik O. Frequency of insulin-dependent diabetes mellitus in Turkish adult-onset diabetic population. Acta Diabetol. 1996; 33:216-9. [19] Lévy-Marchal C, Papoz L, de Beaufort C, Doutreix J, Froment V, Voirin J, Czerni‐ chow P. Clinical and laboratory features of type 1 diabetic children at the time of di‐

[20] Lévy-Marchal C, Patterson CC, Green A; EURODIAB ACE Study Group. Europe and Diabetes. Geographical variation of presentation at diagnosis of type I diabetes in children: the EURODIAB study. European and Dibetes. Diabetologia. 2001 Oct;44

[14] Ali K, Harnden A, Edge J. Type 1 diabetes in children. BMJ 2011;342:d294.

Dec;29(4):657-82.

2001;24: 131– 153.

Nov;75(5):410-5.

2006; 35:725-51.

Suppl. 3:B75-80.

wide 1990-1999. Diabet Med 2006;23:857-66.

betes in Europe. Lancet 2000;355:873-6.).

cet. 2009 Jun 13;373(9680):2027-33.

cemic hyperosmolar state. CMAJ. 2003; 168:859-66.

agnosis. Diabet Med. 1992 Apr;9(3):279-84.
