AN is a 7-year-old male that was rushed into the emergency room on account of abdominal pain, vomiting, fever and altered consciousness, noticed a day prior to presentation.

Abdominal pain was sudden in onset, sharp in character, colicky in nature, more over the epigastrium, non-radiating, not referred, but severe enough to affect child’s activity.

He had several episodes of non-bilious, non-projectile vomiting consisting of recently ingested meals.

At about the same time, he had a low grade on and off fever, worse at night, associated with chills and rigors, and relieved by paracetamol.

He also had a prior history of what parents called “frequent” urination, however no known history of change in the volume or colour of urine. There were 

no associated lower urinary tract symptoms. His appetite was said to have increased but wasn’t gaining weight like his other two obese looking siblings despite his veracious appetite.

He was delivered healthy at term following an uncomplicated pregnancy and is the second child in a non-consanguineous marriage, No known family history of Type-I diabetes or any other chronic illness.

On examination, Child was conscious but drowsy, in mild respiratory distress with Kussmal breathing, tachypneic, with moderate palpebral conjunctival pallor, febrile (Axillary temp [37.7 0 C]), anicteric, severely dehydrated, dry buccal mucosa, sunken eyeballs, very slowly returning skin pinch, prolonged capillary refill time (>3seconds).

Vitals at arrival: T: 37.7 0 C, PR: 120bpm/ min small volume, rapid. Respiratory rate of 40cpm, Sp02: 98% in room air. Abdomen revealed marked Epigastric tenderness, no ascites or organomegally.

CNS: Conscious but drowsy, GCS: 13/1 5 BE:3/4, BV: 5/5, 8M: 5/6

Blood investigations available showed,

unrecordably high random blood glucose >

33.3mmol/dI (Acu-check),

Photospectometric values were 40mM/dI.

Full blood count showed TWBCC: 16.0x

1 O A9 (4-1 Ix 1 O A9) Absolute Neutrophil

(Polymorph) count: 12.12 x 1 0 A 9 (1.6-8.5 x

1 O A9). Packed cell volume: 33.8% (36- 54) Blood Film for Malaria parasites demonstrated asexual forms of P.falciparum (+)

Electrolyte Urea Creatinine: Na+: 1 25

(135-1 50mmoI/I), K+: 4.8mmol/I

(3.5–5.5mmoI/I), Chloride: 94mmoI/I (),

Bicarbonate: 7.1 mmol/l () Urea and serum

Creatinine level was within normal range Urinalysis; Ketone: +++, Glucose: ++, Protein: Trace, Blood: +.

Glycated Haemoglobin was 12% and C-peptide was 0.12.

Therefore, with the findings of polyphagia,? polyuria, hyperglycemia, leukocytosis, elevated HbA1C, low C-Peptide and urinalysis findings of glycosuria and ketonuria, a working diagnosis of DKA precipitated by sepsis? Focus and Malaria were made. Management immediately commenced, 2 IV accesses were secured for I.V fluid and insulin administration. He received about 2700mIs over 2-4hrs. The child commenced on soluble insulin after the first hour of fluid resuscitation 0.1 IU per kg/hr as a continuous infusion with hourly RBG monitoring. In addition, IV KCL was added to the IVF 1 OMEq/L after the second hour of fluid resuscitation and review of his serum potassium level (>3.5mM/L).

Injection Ceftriaxone +Tazobactam

(100mg/kg in 2 divided doses), I.V

Artesunate (Rekmal) 2.4mg/kg (64.8mg_)

@ 0, 1 2, 24hrs were also commencd. Child

was maintained on NPO until he was out of ketotic state evidenced by absence of ketonuria, regaining full consciousness and good sugar control. Vital signs and GCS were closely monitored.

Following the reduction of his RBG to < 14mM/dI, IVF N/S was changed to 5% D/S and insulin dosage reduced to 0.051U/Kg/ HR with sustenance of hourly RBS monitoring.

With his subsequent recovery of consciousness and clearance of ketonuria, he was encouraged to commence feeding with pre meal subcut soluble insulin 301U given 30minutes before his meals.

Random blood sugar was monitored at

4hourIy interval, values fluctuated between 3.8 and 14mmoI/dI. This was due to his high caloric intake and informed the invitation of a dietician. Dietary counsel and modification were instituted by the Dietician with improvement in glycaemic control. He later commenced on a dual acting insulin (Mixtard) on the 4th day on admission and was later discharged on the 6th day following good glycaemic control and thorough counselling on the chronic nature of the condition, needed for compliance with medications, dietary plan and follow up visits.

He is doing well on medications and has been seen on a follow-up visit with good compliance on dietary plan and subcutaneous insulin. Blood sugar ranging between 3.8 and 8.0mM/dI.

This case emphasizes that DKA can occur even in children with a previously obese phenotype, challenging the common association of obesity with only Type 2 diabetes.

On admission