Severe Diabetic Ketoacidosis With Leukemoid Reaction and Coma in a Toddler: A Case Report

Abstract

We present a case of a 3-year-old girl with previously diagnosed type 1 diabetes mellitus (T1DM) who was admitted in an unconscious state with severe diabetic ketoacidosis (DKA), lactic acidosis, and coma. The condition was complicated by profound dehydration, leukemoid reaction of neutrophilic type, and reactive thrombocytosis. Early intensive care management, mechanical ventilation, and insulin therapy led to stabilization and gradual recovery. This case highlights the critical importance of early recognition, aggressive management, and multidisciplinary care in pediatric patients with complicated DKA.

Introduction

Type 1 diabetes mellitus (T1DM) is a chronic autoimmune condition characterized by the destruction of pancreatic beta cells, leading to absolute insulin deficiency. It typically presents in childhood or adolescence and requires lifelong insulin therapy. However, recent epidemiological data have shown that more than half of all new incidences of type 1 diabetes occur in adulthood. Key genetic, immune, and metabolic differences exist between adult- and childhood-onset type 1 diabetes, many of which are not well understood. ¹ Without appropriate management, T1DM can result in acute complications such as diabetic ketoacidosis (DKA), which is the leading cause of morbidity and mortality in children with diabetes. DKA is characterized by hyperglycemia, ketonemia, metabolic acidosis, and clinical dehydration.^1,2

In pediatric patients, DKA can progress rapidly and is often the initial presentation of undiagnosed diabetes. ³ It can also occur due to missed insulin doses, intercurrent illness, or psychosocial factors interfering with proper disease management. Early symptoms such as polyuria, polydipsia, and weight loss may go unrecognized until severe metabolic derangement occurs. In rare cases, DKA may be accompanied by hematologic abnormalities such as leukemoid reactions and reactive thrombocytosis, which are generally associated with a systemic inflammatory response.^3-5

Despite improvements in diabetes management, DKA remains a serious condition associated with significant rates of death, highlighting the need for early detection and timely intervention.

DKA develops due to insulin deficiency, which may result from progressive destruction of pancreatic beta cells in previously undiagnosed T1DM, or from treatment interruptions during infections, surgery, trauma, or psychological stress. This insulin lack leads to excessive glucose production by the liver and kidneys, reduced glucose uptake in tissues, and increased fat breakdown, driving ketone production. Counter-regulatory hormones, that is, cortisol, glucagon, catecholamines, and growth hormone can exacerbate hyperglycemia and ketogenesis by enhancing gluconeogenesis, glycogen breakdown, and lipolysis. The predominant ketone body, beta-hydroxybutyrate, plays a central role in metabolic acidosis. ²

Elevated blood glucose levels trigger osmotic diuresis, causing significant dehydration and disturbances in electrolytes such as sodium, potassium, chloride, calcium, phosphate, and magnesium. These changes in turn reduce kidney perfusion and glomerular filtration rate, worsening hyperglycemia.^1-3 In addition, inflammatory cytokines and oxidative stress lead to the insulin secretion and action impairment. At the same time free fatty acids can disrupt vascular function by reducing nitric oxide availability. If left untreated, DKA can lead to severe complications, multiple organ failure, and death. ⁶

In high-income countries, mortality from pediatric DKA is relatively low (0.15%-0.3%), but it increases significantly when complications arise. Cerebral edema (CE) is the most dangerous complication, occurring in 0.3% to 1% of cases and associated with a high fatality rate (20%-30%). ⁷ Children with CE have a mortality rate of 6.4%, compared to 0.1% in those without. Acute kidney injury (AKI) occurs in 30% to 64% of children with severe DKA, often beginning as pre-renal due to low blood flow and potentially progressing to intrinsic kidney damage such as acute tubular necrosis.^6,7

Acute respiratory distress syndrome (ARDS) is another rare but serious complication. It involves sudden respiratory failure and low oxygen levels, likely due to inflammation, capillary leakage, and pulmonary edema caused by severe acidosis and hyperglycemia-induced cytokine release. ⁸

Gastrointestinal complications such as non-occlusive mesenteric ischemia may occur due to poor intestinal blood flow and vascular injury. Additionally, DKA can affect cognitive development in young children, particularly those under 5, increasing the risk of long-term impairments in memory, attention, and intelligence even in the absence of obvious neurological symptoms. ⁹

This report discusses the case of a 3-year-old girl presenting with severe DKA, coma, and hematologic complications. The case underscores the importance of early diagnosis, the role of intensive care in management, and the need to address social determinants of health in children with chronic diseases.

Case Presentation

A 3-year-old girl was brought to the emergency department by emergency medical services on September 4, 2024, in an unconscious state. She had a known history of Type 1 Diabetes Mellitus, but her adherence to insulin therapy was unclear. On admission, she was comatose (Glasgow Coma Scale [GCS] score of 8), presenting with Kussmaul breathing, severe hyperglycemia (>30 mmol/L), and signs of profound dehydration. Oxygen therapy was initiated at 5 L/min via nasal cannula.

Although T1DM was confirmed, details of her insulin regimen were unknown. Her clinical examination revealed no focal neurological deficits. Pupils were equal, round, and reactive to light. Meningeal signs were absent. Skin appeared pale, mucous membranes were pink and dry, and her tongue was also dry. Capillary refill time was 3 seconds. Vital signs including a heart rate of 160 bpm, blood pressure ranging from 116/66 to 124/72 mmHg, and tachypnea were documented. Lung auscultation revealed harsh breath sounds. The abdomen was symmetrical and soft, with no hepatosplenomegaly. A nasogastric tube was inserted and drained “coffee ground” material.

Under aseptic conditions and ketamine sedation (100 mg IM), a central venous catheter was inserted into the left brachiocephalic vein. Bedside ultrasound revealed preserved pleural sliding, no fluid collections, normal left ventricular function, no pericardial effusion, and a collapsible inferior vena cava on inspiration.

Laboratory findings showed severe metabolic acidosis (pH < 6.9, pCO₂ 19.0 mmHg, base excess and bicarbonate unmeasurable), hyperglycemia (27.6-32.0 mmol/L), lactic acidosis (3.4 mmol/L), marked hyperketonemia, and hyperkalemia (5.4 mmol/L). Liver function was within normal limits; renal function was preserved. HbA1c was 10%. Complete blood count (CBC) revealed marked leukocytosis (WBC 76.7 × 10⁹/L) with myelocytes (10%), metamyelocytes (6%), band forms (10%), neutrophils (27%), eosinophils (18%), lymphocytes (21%), and thrombocytosis (PLT 524 × 10⁹/L). Urinalysis showed high specific gravity (1047), 4+ acetone, proteinuria (0.086g/L), 2+ urates, and no signs of infection. Plasma osmolarity was 318 mOsmol/kg.

The patient was transferred to the intensive care unit (ICU). Initial management of diabetic ketoacidosis (DKA) included 0.9% NaCl at 10 mL/kg over 1 hour. Fluid therapy was continued with 0.9% NaCl containing 20 mmol/L KCl, administered after confirming urine output. Insulin therapy was initiated 2 hours later as a continuous intravenous infusion at 0.1 IU/kg/hour.

Despite 12 hours of intensive therapy, the patient showed no significant improvement. Severe metabolic acidosis persisted (pH 7.01, base excess −23, HCO₃ 4.5 mmol/L), and her GCS declined to 7. She was intubated with a 4.5 mm cuffed endotracheal tube and placed on mechanical ventilation using a Fabius machine. Hemodynamic parameters remained stable.

Subsequently, the patient was transferred to another ICU and placed on an Aveo ventilator in SIMV mode with FiO₂ of 35%. Laboratory tests showed elevated CRP (25.17 mg/L), WBC (60.4 × 10⁹/L), and PLT (516 ×10⁹/L). A hematology consultation diagnosed a neutrophilic leukemoid reaction and reactive thrombocytosis. Dipyridamole was prescribed at 3 mg/kg/day, with recommendations for ongoing CBC monitoring, antibiotics, and continued infusion therapy. Within 24 hours of ICU transfer, the patient’s condition remained critical but began to improve. Thiopental sodium infusion was discontinued. She was extubated and transitioned to subcutaneous Actrapid insulin (1 IU/kg/day). On examination, her GCS had improved to 12, and she was responsive to stimuli. She had a mild fever (37.2°C) and was breathing effectively on 2 L/min oxygen. CBC showed improvement, with WBC reduced to 25.4 × 10⁹/L, normalization of neutrophil counts, and platelets decreased to 258 × 10⁹/L.

Over the following 24 hours, her condition stabilized. She was responsive, afebrile (36.8°C-37.8°C), breathing independently on room air, receiving enteral feeding via nasogastric tube, and maintaining adequate urine output (1.7 mL/kg/hour). Laboratory tests revealed blood glucose levels ranging from 5.3 to 14.4 mmol/L, mild hypokalemia (3.22 mmol/L), and a compensated metabolic state (pH 7.39, HCO₃ 24.8 mmol/L). CBC showed WBC 11.6 × 10⁹/L and Hb 101 g/L.

In summary, treatment included fluid therapy (2391 mL), oxygen therapy, mechanical ventilation, sedation (Thiopental sodium), sodium bicarbonate 4%, intravenous and subcutaneous Actrapid, omeprazole, oral hygiene, Cytomax eye drops, lactulose 10 mL orally, dipyridamole (1 tablet 3 times daily), symptomatic therapy, electrolyte correction, and continuous clinical monitoring.

At discharge, laboratory tests showed significant improvement: RBC 4.3 × 10¹²/L, Hb 111 g/L, Hct 0.34, PLT 179 × 10⁹/L, WBC 7.4 × 10⁹/L, urea 4.9 mmol/L, creatinine 25 µmol/L, glucose 14.5 mmol/L, amylase 98 U/L, potassium 4.4 mmol/L, sodium 139 mmol/L, calcium 1.1 mmol/L, chloride 102.5 mmol/L, pH 7.37, pCO₂ 31.9 mmHg, and HCO₃ 18.5 mmol/L. A summary of key laboratory parameters throughout the hospital stay is provided in Table 1.

Table 1.

Summary of the Basic Laboratory Tests.

Parameter	At the admission to hospital	12 h in ICU	24 h in ICU	48 h in ICU	Discharge from hospital
WBC count, 10⁹/L	76.7	60.4	25	11.6	7.4
PLT count, 10⁹/L	524	516.33	258	—	179
CRP, mg/L	—	25.17	—	—	—
Serum K, mmol/L	5,4	—	—	3,22	4.4
Blood pH	<6.9	7.01	—	7.39	7.37
HCO₃	Unrecordable	4.5	—	24.8	18.5

Final diagnosis at discharge from hospital was: Type 1 Diabetes Mellitus, DKA, lactic acidosis. Coma (E10.16). Dehydration. Leukemoid reaction of neutrophilic type, reactive thrombocytosis, hyperleukocytosis. Purulent conjunctivitis. “Black esophagus.”

Discussion

This case illustrates a fulminant presentation of diabetic ketoacidosis DKA in a very young child, highlighting the serious risk posed by inadequate diabetes management and lack of social support.^10-12 The presence of a leukemoid reaction is unusual in pediatric DKA and suggest severe background metabolic shifts. Leukemoid reactions, though rare, can occur in response to severe infections, metabolic disturbances, and significant physiologic stress. In this case, the child’s leukemoid reaction, with a marked left shift, was confirmed by hematologic consultation to be reactive in nature.^11-15

In general the hematologic abnormalities in pediatric DKA are not uncommon and often reflect dehydration, acidosis, or underlying infections. Common findings include leukocytosis, which is frequently reactive and related to stress or inflammation rather than infection. ¹⁶ Hemoconcentration due to volume depletion can result in elevated hematocrit, mild thrombocytosis may also be observed. More severe or rare hematologic complications include disseminated intravascular coagulation (DIC), thrombotic events, and hemolysis in cases with underlying glucose-6-phosphate dehydrogenase (G6PD) deficiency. The leukemoid reaction observed in our case is rare in DKA and underscores the importance of recognizing extreme physiological stress responses in critically ill pediatric patients. Children with DKA frequently exhibit leukocytosis, often due to stress, infection, or inflammation.^15,17 The leukemoid reaction observed in our patient is an uncommon manifestation, underscoring the complexity and variability of hematologic responses in pediatric DKA. ¹⁷

The pathophysiological mechanisms are not fully elucidated but are believed to involve the intense systemic inflammatory milieu induced by severe metabolic disturbances, including acidosis and hyperosmolality. Elevated pro-inflammatory cytokines (eg, IL-6, TNF-α) in such conditions may stimulate myelopoiesis and megakaryopoiesis, explaining both neutrophilia and thrombocytosis. ¹⁸ In this patient, the absence of infection and the normalization of counts with supportive care support a reactive, non-malignant etiology.

The utility of hematology consultation in differentiating reactive versus malignant processes cannot be overstated, especially in resource-limited or high-stakes acute settings where misdiagnosis may lead to unnecessary interventions.

The management of severe DKA in children requires a multidisciplinary approach involving pediatric intensivists, endocrinologists, and supportive specialties such as hematology and neurology. Prompt fluid resuscitation, careful insulin therapy, and ventilatory support were critical in stabilizing the patient. The use of thiopental sodium for sedation helped synchronize the patient with mechanical ventilation, which may be lifesaving in cases of coma and respiratory compromise.^3,5,10 The role of early mechanical ventilation in preserving cerebral perfusion and oxygenation during profound metabolic acidosis is particularly important in cases like this, where Glasgow Coma Scale scores suggest impending or ongoing cerebral edema. Although no neuroimaging was documented, clinical vigilance and neuroprotective strategies were key. ¹⁰

This case also raises awareness of the importance of acid-base correction and electrolyte monitoring. Hypokalemia developed during treatment, which is a known complication during the resolution phase of DKA as insulin promotes intracellular potassium shift. Monitoring potassium closely and providing timely correction helped prevent arrhythmias and neuromuscular dysfunction.

Furthermore, gastrointestinal symptoms, that is, such as the “coffee ground” aspirate—warrant consideration. Stress-related mucosal disease or DKA-associated gastritis could account for this presentation. Prophylactic omeprazole likely mitigated the risk of gastrointestinal bleeding and should be considered in similar severe presentations.

Acute esophageal necrosis (AEN), also referred to as “black esophagus,” is a rare but potentially life-threatening complication of the DKA. It is most often seen in critically ill patients and is associated with tissue hypoperfusion, impaired mucosal defense, and acid reflux. ¹⁹ In the context of DKA, severe dehydration, metabolic acidosis, and hemodynamic instability may contribute to esophageal ischemia and mucosal injury, increasing the risk of AEN. Clinical manifestations include hematemesis or the presence of “coffee ground” material in gastric aspirate. Diagnosis is typically confirmed via upper endoscopy. Management is supportive and includes hemodynamic stabilization, proton pump inhibitor therapy (ie, omeprasol, administered in our study), with a focus on preventing complications such as perforation or strictures.^19,20

The patient’s social background likely contributed to delayed diagnosis and inadequate diabetes control. Social determinants of health, including poverty, neglect, and lack of caregiver knowledge—remain major challenges in the management of chronic conditions in children. Healthcare systems must account for these factors and ensure adequate follow-up and support services for vulnerable pediatric populations. Pediatric diabetes care must extend beyond clinical management to include structured education, regular outreach, and social work support. Multidisciplinary clinics that incorporate diabetes educators and psychosocial services have been shown to reduce readmissions and improve glycemic control in vulnerable populations.

The improvement in clinical and laboratory parameters over a short hospital stay highlights the effectiveness of well-coordinated critical care. Normalization of the patient’s glucose levels, acid-base balance, and hematologic profile following appropriate therapy underscores the importance of early, aggressive, and comprehensive management of complicated DKA. While leukemoid reaction in DKA is rare, its recognition is crucial to avoid misinterpretation as leukemia or severe sepsis. Furthermore, this case underlines the importance of comprehensive baseline investigations in all pediatric DKA admissions—including complete blood counts with differentials—to capture atypical findings that may influence management.

Lastly, the case reinforces the necessity of clear discharge planning, insulin regimen education, and long-term endocrinology follow-up to prevent recurrence. Community-based follow-up programs and integration of telemedicine may offer scalable solutions in low-resource or high-risk populations. Public health initiatives should also aim to improve early detection of diabetes in young children and reduce diagnostic delays, which remain a key factor contributing to DKA-related hospitalizations (Figure 1).

Figure 1.

Summarized scheme of the clinical case.

The improvement in clinical and laboratory parameters over a short hospital stay highlights the effectiveness of well-coordinated critical care. Normalization of the patient’s glucose levels, acid-base balance, and hematologic profile following appropriate therapy underscores the importance of early, aggressive, and comprehensive management of complicated DKA.

Potential study limitations of this study need to be discussed. The absence of neuroimaging limited our ability to definitively assess for cerebral edema, and the diagnosis of acute esophageal necrosis was based on clinical presentation without endoscopic confirmation. Additionally, detailed information on the patient’s pre-hospital insulin regimen, adherence, and social background was limited to caregiver report. Finally, the lack of long-term follow-up data prevents assessment of potential neurocognitive or metabolic disorders after discharge.

Conclusions

Severe DKA in pediatric patients may present with multisystem involvement, including hematological complications. Early recognition and aggressive intervention are crucial. This case also underscores the importance of social determinants of health in managing chronic diseases in children.