On the edge of severe DKA: A survival story

Anne Prewina Gurushekar¹, Sivaprakash², Kavu Devi³, Sai³

¹Consultant Pediatrician, Kauvery Hospital, Tirunelveli, Tamil Nadu

²Consultant Endocrinologist, Kauvery Hospital, Tirunelveli, Tamil Nadu

³Critical Care Team, Kauvery Hospital, Tirunelveli, Tamil Nadu

Abstract

Severe diabetic ketoacidosis (DKA) in children is a life-threatening emergency requiring meticulous fluid, electrolyte, and insulin management.

We report the case of an 11-year-old girl with severe DKA and profound acidosis (pH 6.8) who was managed successfully without bicarbonate therapy. She was treated as per ISPAD guidelines. Real-time POCUS assessment of IVC collapsibility as well as CVP monitoring proved pivotal in optimizing fluid replacement. The patient recovered fully and was discharged on a basal-bolus insulin regimen.

Keywords: Pediatric diabetic ketoacidosis, severe acidosis, bicarbonate therapy, POCUS, case report.

Introduction

Diabetic ketoacidosis (DKA) is a serious and potentially fatal complication of diabetes mellitus in children, characterized by hyperglycemia, metabolic acidosis, and ketonemia. Severe acidosis (pH <7.0) is associated with increased morbidity and mortality, often due to cerebral edema and electrolyte disturbances.

While fluid resuscitation and insulin therapy remain the mainstay of treatment, adjunctive bicarbonate therapy has been debated for decades. Studies suggest that bicarbonate offers no clinical benefit and may increase the risk of paradoxical central nervous system (CNS) acidosis, hypokalemia, and cerebral edema ^(1–3,5).

POCUS assessment of IVC collapsibility, though not routinely used in pediatric DKA, can aid in tailoring fluid therapy in severe dehydration.

Case Presentation

An 11-year-old well-thriving girl presented with severe abdominal pain and vomiting. She had polydipsia and polyuria for several weeks, which were overlooked. An abdominal ultrasound done at another private hospital showed mesenteric lymphadenitis, and she was admitted there for four days on account of severe abdominal pain. On day four, she developed giddiness and drowsiness. Random blood glucose was 489 mg/dL, and she was immediately referred to our center.

On arrival, she was drowsy but responsive to verbal commands (GCS 14: E3V5M5). She was tachycardic (HR 122 bpm), borderline hypotensive (BP 100/50 mmHg), and had faint peripheral pulses. She had severe dehydration with sunken eyes and dry tongue. Pupils were reactive, with no focal neurological deficits. Arterial blood gas revealed severe metabolic acidosis (pH 6.8, bicarbonate <3 mmol/L) with high anion gap (anion gap 33.7 mEq/L). Urine ketones were positive, and random blood glucose exceeded 500 mg/dL.

Two peripheral IV lines were secured, and a nasogastric tube was inserted. Normal saline boluses (10 mL/kg) were given twice initially in the first hour. Serum sodium was 132 mEq/L and potassium 4.7 mEq/L. After one hour of fluid resuscitation, insulin infusion was started at 1 U/kg/hour, targeting a glucose reduction of 50–75 mg/dL/hour. Sepsis was ruled out.

POCUS revealed a collapsible IVC, prompting additional boluses. Deficit plus maintenance fluids (normal saline with potassium chloride initially, later half-normal saline with potassium chloride) were administered over 48 hours. When potassium dropped below 3 mEq/L, insulin was paused temporarily, and potassium supplementation (60 mmol/L) was given.

A central venous catheter was placed for access along with CVP monitoring, and serial POCUS assessments guided fluid boluses during the first 48 hr. She needed several boluses of fluid in the first 24 hr. For monitoring, venous blood gases and electrolytes were checked every 6 hours. By 48 hours, pH improved to 7.2 and bicarbonate to 17 mmol/L. Her sensorium normalized only by day 2, and she tolerated oral intake.IV fluids were tapered after 48 hours and Insulin was transitioned to subcutaneous glargine once daily and rapid-acting analog with meals. Her GAD 65 antibodies were more than 2000 U/ml and she was diagnosed as Type 1 Diabetes. She was discharged on day five and remains stable on follow-up.

Discussion

Role of Bicarbonate

Despite profound acidosis (pH 6.8), bicarbonate therapy was not given. Pediatric DKA guidelines advise against routine bicarbonate due to risks such as paradoxical CNS acidosis, hypokalemia, and increased cerebral edema ^(1–3). Retrospective studies associate bicarbonate with prolonged hospitalization and no outcome improvement ⁽²⁾. This case supports managing severe acidosis with fluids and insulin while closely monitoring gases and electrolytes. Bicarbonate is now recommended only for children WITH severe circulatory failure and a high risk of cardiac decompensation due to profound acidosis ⁽⁴⁾. In our case the gradual improvement in acidosis proved reassuring

Role of POCUS and IVC Collapsibility

The patient’s severe dehydration and hemodynamic compromise required careful fluid titration and was challenging especially in the first 24 hr. POCUS-guided IVC assessment as well as CVP monitoring enabled tailored bolus administration, likely preventing under-resuscitation or overload. Although not routine in pediatric DKA, this method can be a useful tool in severe or unstable cases.

Conclusion

This case underscores two critical principles in severe pediatric DKA management:

Routine bicarbonate therapy is unnecessary and may be harmful in children, even with profound acidosis, unless clearly indicated.
POCUS-guided IVC assessment can be valuable for optimizing fluid resuscitation in severe or unstable cases.

References

Chua HR, Schneider A, Bellomo R. Bicarbonate in diabetic ketoacidosis—a systematic review. Ann Intensive Care. 2011; 1:23.
Green SM, Rothrock SG, Ho JD, Gallant RD, Borger R, Thomas TL, Zimmerman GJ. Failure of adjunctive bicarbonate to improve outcome in severe pediatric diabetic ketoacidosis. Ann Emerg Med. 1998;31(1):41–48.
Patel M, Afifi AM, Hercher RL, Moussa M. Reevaluating bicarbonate therapy in pediatric DKA: A propensity score-matched analysis of neurological and respiratory outcomes. Am J Emerg Med. 2025; 75:58–64.
Glaser N, Barnett P, McCaslin I, Nelson D, Trainor J, Louie J et al. Risk factors for cerebral edema in children with diabetic ketoacidosis. The Pediatric Emergency Medicine Collaborative Research Committee of the American Academy of Pediatrics. N Engl J Med. 2001 Jan 25;344(4):264-9.

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On the edge of severe DKA: A survival story