Severe pediatric diabetic ketoacidosis with multi-organ dysfunction and complete recovery in a resource-limited setting: A case report

Abstract

BACKGROUND

Diabetic ketoacidosis (DKA) remains the most serious acute complication of type 1 diabetes mellitus (T1DM) in children and adolescents and is associated with significant morbidity and mortality when complicated by multi-organ failure.

CASE SUMMARY

We report the case of a 12-year-old girl with established T1DM who presented with profound DKA complicated by acute kidney injury (AKI) requiring haemodialysis, recurrent generalized seizures, cerebral oedema, and haemodynamic instability. Serial blood-gas analyses demonstrated extreme metabolic acidosis with persistently low bicarbonate levels despite standard therapy. Through aggressive multidisciplinary management involving paediatric intensive care, endocrinology, nephrology, neurology, and rehabilitation services, the patient achieved complete neurological, metabolic and renal recovery.

CONCLUSION

Pediatric DKA is life-threatening, with higher mortality in resource-limited settings due to complications like cerebral edema and AKI. Cerebral edema is the leading cause of death, requiring rapid treatment with mannitol or hypertonic saline. AKI is common, increases mortality and hospital stay, and may progress to chronic kidney disease. Early recognition of risk factors, prompt treatment, and close follow-up are critical to improving outcomes.

Key Words: Diabetic ketoacidosis; Acute kidney injury; Intensive care unit; Multi-organ dysfunction; Hemodialysis; Case report

Core Tip: Severe diabetic ketoacidosis (DKA) in children can progress rapidly to life-threatening multi-organ dysfunction. We describe a 12-year-old girl with type 1 diabetes mellitus who developed acute kidney injury requiring haemodialysis, cerebral oedema, seizures, and haemodynamic instability during DKA. Despite cardiac arrest and prolonged intensive care, the patient achieved complete neurological and renal recovery through aggressive multidisciplinary management. This case highlights that early recognition of complications, timely critical care intervention, and coordinated specialty care can result in favourable outcomes even in severe paediatric DKA in resource-limited settings.

INTRODUCTION

Diabetic ketoacidosis (DKA) is a life-threatening emergency and remains a leading cause of diabetes-related mortality in children with type 1 diabetes mellitus (T1DM)[1]. Severe DKA may be complicated by cerebral oedema, acute kidney injury (AKI), electrolyte disturbances, seizures, and cardiovascular instability, each of which independently worsens prognosis[2]. Although most cases respond to standard fluid and insulin protocols, a subset progresses to refractory metabolic derangements requiring advanced organ support. We describe a pediatric case of severe DKA complicated by cerebral oedema, recurrent seizures, dialysis-dependent AKI, haemodynamic instability, cardiac arrest, and prolonged intensive care admission, with eventual complete neurological and renal recovery following multidisciplinary management in a resource-limited setting. This case highlights the challenges and potential for favorable outcomes in critically ill pediatric patients despite severe multi-organ dysfunction.

CASE PRESENTATION

Chief complaints

A 12-year-old girl with a three-year history of T1DM presented with a four-day history of chest pain, fever, polyuria, polydipsia and progressive generalized weakness.

History of present illness

She had initially been admitted to a peripheral hospital with a diagnosis of DKA and commenced on insulin therapy. However, her clinical condition deteriorated, prompting referral to our tertiary centre. Reduced oral intake and possible disruption of insulin administration during the acute illness may have contributed to the development of DKA.

History of past illness

The patient had a three-year history of T1DM managed on insulin therapy, with no previous history of severe DKA, chronic kidney disease, seizures, or other known chronic medical conditions.

Personal and family history

No family history of diabetes, other chronic illnesses or consanguinity.

Physical examination

On admission, she appeared acutely ill and severely dehydrated, with Kussmaul respirations and a depressed level of consciousness. Her Glasgow Coma Scale (GCS) score was 10/15 (E2 V2 M6), with no focal neurologic deficits.

Laboratory examinations

Capillary blood glucose was markedly elevated at 20.1 mmol/L, and venous blood-gas analysis revealed a metabolic acidosis with a pH of 6.94, bicarbonate levels of 1.7 mmol/L, and 3+ ketonuria. Figure 1 shows the evolution of laboratory parameters over time.

Figure 1  pH and bicarbonate trends.

Imaging examinations

Electroencephalography demonstrated diffuse cerebral slowing. Neuroimaging findings were consistent with cerebral oedema. Renal ultrasonography performed on day 24 revealed bilaterally increased cortical echogenicity with reduced corticomedullary differentiation, consistent with resolving parenchymal renal injury.

MULTIDISCIPLINARY EXPERT CONSULTATION

Due to worsening metabolic acidosis, persistent anuria, haemodynamic instability, and neurological deterioration, multidisciplinary input was sought from paediatric intensive care, nephrology, neurology, endocrinology, nutrition and physiotherapy teams. Following specialist review on day 3 of admission, haemodialysis was recommended for refractory metabolic acidosis and stage 3 AKI. Neurology consultation followed the onset of seizures and cerebral oedema.

FINAL DIAGNOSIS

Severe DKA complicated by cerebral oedema, recurrent generalized tonic-clonic seizures, stage 3 AKI requiring hemodialysis, hemodynamic instability, cardiac arrest and respiratory failure requiring mechanical ventilation.

TREATMENT

Initial management in the emergency department focused on rapid haemodynamic stabilization and correction of metabolic derangements. Intravenous fluid resuscitation with normal saline at 20 mL/kg was initiated within the first hour. This was followed by an infusion of intravenous insulin at 0.1 units/kg/hour and a maintenance infusion of saline and dextrose-normal saline, depending on the blood sugar. The patient was transferred to the intensive care unit (ICU) where treatment was continued. Potassium chloride (20 mEq) was also added to each 500 mL of normal saline. In the ICU, mannitol was administered at 40 g every 30 minutes for three doses due to concern about cerebral oedema. A urinary catheter was inserted for urine output monitoring, bedside capillary glucose measurements were performed hourly, and supplemental oxygen was delivered via a non-rebreather mask. Empiric antimicrobial therapy with ceftriaxone (1 g every 12 hours) was initiated.

By the third day of admission, the patient developed persistent oliguria progressing to complete anuria for more than 24 hours. Laboratory investigations demonstrated severe AKI, with serum creatinine of 297 μmol/L and urea of 14.2 mmol/L (Table 1). Marked electrolyte derangements were noted, including, hypochloraemia, hypophosphataemia, hypocalcaemia, mild hyponatremia and magnesium imbalance (Table 2). Inflammatory markers were markedly elevated early in the course, with C-reactive protein peaking at 111.5 ng/mL and procalcitonin at 23.62 ng/mL, both of which steadily declined in response to treatment.

Table 1 Renal function.

	Reference range	D3	D4	D5	D6	D7	D8	D12	D19	D22	D24	D29	D31	D34
Urea (mmol/L)	1.8-5.2	14.2	19.9	24.7	22.9	20.5	13.9	31.8	13.7	7.2	5.3	6.7	4.7	5.0
Creatinine (µmol/L)	20-70	297	557	576	500	470	371	666	457	290	194	104	83	74

Table 2 Electrolyte changes.

Parameter (unit)	Reference range	D1	D2	D3	D4	D5	D6	D7	D8	D9	D12	D19	D24	D29
Na (mmol/L)	136-145	136	147	143	139	143	138	134.4	135	141	137	139	141	136
K (mmol/L)	3.5-5.5	3.9	3.8	4.2	3.5	3.2	3.3	4.2	3.9	2.9	4.0	5.0	3.2	4.4
Cl (mmol/L)	96-108	115	128	133	126	119	112	103	104	106	103	102	104	98

The patient required vasopressor support with adrenaline (0.06-0.3 µg/kg/minute) for haemodynamic instability. On assessment, her body mass was 43 kg, was afebrile (37 °C), and had a blood pressure of 115/56 mmHg (mean arterial pressure 73 mmHg), respiratory rate of 37 breaths/minute, oxygen saturation of 96% on 2 L/minute via nasal prongs, and a bedside glucose of 18.4 mmol/L. Thyroid function tests showed low free T4 and free T3 with a normal thyrotropin, consistent with euthyroid sick syndrome. Serum cortisol levels were not evaluated during admission. However, the patient’s haemodynamic instability was attributed to severe DKA, sepsis, and multi-organ dysfunction, with subsequent clinical improvement following supportive management. Coagulation studies revealed a mildly prolonged prothrombin time with normal international normalized ratio and activated partial thromboplastin time. Serological testing for human immunodeficiency virus, hepatitis B, and hepatitis C was negative. Despite prompt and appropriate management of DKA, including aggressive fluid resuscitation, continuous insulin infusion, oxygen therapy, and close biochemical monitoring, the patient’s renal function continued to deteriorate and advanced to stage 3 AKI with refractory metabolic acidosis and persistent anuria. Due to poor biochemical response to standard therapy, bicarbonate therapy was initiated in the setting of severe metabolic acidosis with haemodynamic instability and worsening renal failure. Following multidisciplinary review, intermittent haemodialysis via a 7-French femoral dual-lumen catheter was commenced. Dialysis was performed on alternate days, with approximately ten sessions required before renal recovery was observed.

Between days 3 and 6 of admission, the patient experienced two witnessed generalized tonic-clonic seizures. Electroencephalography demonstrated diffuse cerebral slowing, and neuroimaging findings were consistent with cerebral oedema. She was treated with intravenous levetiracetam and hypertonic (3%) saline, resulting in gradual neurological improvement. On day 6, the patient suffered a cardiac arrest and was successfully resuscitated. Contributing factors included severe metabolic acidosis, anaemia, azotaemia, and profound hypophosphataemia. Management included packed red blood cell transfusion (10 mL/kg), aggressive electrolyte replacement, bicarbonate therapy and continuation of insulin infusion. Dexamethasone was administered as adjunctive therapy during the period of severe cerebral oedema. Potassium supplementation and escalation of vasopressor support were also undertaken. She subsequently developed hypoxaemia requiring endotracheal intubation and mechanical ventilation in the ICU.

Analgesia-sedation was provided with fentanyl. Chest physiotherapy was initiated, and she received total parenteral nutrition. Serial laboratory investigations demonstrated dynamic haematological, inflammatory, and hepatic changes during admission. The white blood cell count fluctuated markedly, rising from normal values to a peak of 20.5 × 10⁹/L, consistent with a significant inflammatory or infectious response, before normalising with clinical improvement. Haemoglobin levels progressively declined from 11.0 g/dL to a nadir of 6.3 g/dL, reflecting severe anaemia that later improved following transfusion and recovery, reaching 11.7 g/dL at discharge. Platelet counts were initially low-normal but subsequently increased, peaking at 444 × 10⁹/L, before stabilising. On day 7, serum calcium had decreased to 2.08 mmol/L and phosphate to 0.94 mmol/L, both of which, were corrected. Serial arterial blood-gas analyses demonstrated gradual and sustained correction of metabolic acidosis, with pH and bicarbonate levels returning toward normal. Serial serum or urine ketone measurements were not consistently performed during admission. Resolution of DKA was monitored using serial blood glucose measurements, improvement in metabolic acidosis, bicarbonate levels, and clinical status. Glycaemic control stabilised with ongoing insulin titration.

Antimicrobial therapy was escalated to piperacillin-tazobactam. Blood cultures remained sterile, while tracheal aspirate cultures grew Staphylococcus aureus sensitive to clindamycin, prompting antibiotic de-escalation. Due to the prolonged intensive care admission, reduced mobility and presence of a femoral dialysis catheter, thromboprophylaxis with enoxaparin was initiated to reduce the risk of thromboembolism. Additionally, physiotherapy, early mobilisation, and nutritional rehabilitation was also administered as supportive therapy. By day 10, the patient was successfully weaned off ventilatory and vasopressor support and discharged from the paediatric ICU.

The patient remained stable on the ward, maintaining oxygen saturations above 90% on room air, fully oriented with a Glasgow Coma Scale score of 15/15, and tolerating oral feeds. On day 24, renal ultrasonography revealed bilaterally increased cortical echogenicity with reduced corticomedullary differentiation, consistent with resolving parenchymal renal injury. Renal function steadily improved, with urea decreasing to 5.3 mmol/L and creatinine to 194 μmol/L by day 24, further improving to 41 μmol/L by day 27. Supportive care included blood transfusion for anaemia, nutritional rehabilitation, physiotherapy and early mobilisation. The patient was discharged home on day 37 post-admission in stable condition, with urea 2.8 mmol/L, creatinine 58 μmol/L, haemoglobin 9.2 g/dL, bicarbonate 24 mmol/L, and on a basal-bolus insulin regimen.

OUTCOME AND FOLLOW-UP

After 37 days of inpatient care (10 days in the ICU and 27 days in the paediatric endocrine ward) the patient demonstrated marked clinical improvement, with recoverymonstrated marked clinical improvement, with recovery of urine output, improving renal indices, and complete neurological recovery. Comprehensive diabetes education was reinforced for both the patient and her caregiver, and structured outpatient follow-up was arranged to monitor glycaemic control, renal function, and psychosocial adjustment (Table 3).

Table 3 Timeline of treatment.

Time	Treatment
Day 1	Admission to ICU with severe DKA, shock severe acidosis and ketonuria
Day 2	Standard DKA management
Day 3	Worsening oliguria progressing to anuria
	Care was transferred under specialists
	Hemodialysis indicated
Day 4-6	Two episodes of generalized tonic clonic seizures
	Neuroimaging indicated and cerebral oedema was noted
	Mannitol, hypertonic saline and levetirecetam
Day 6	Cardiac arrest secondary to metabolic derangements and multi-organ dysfunction
	Successful resuscitation and the patient was intubated and mechanically ventilated
Day 7-10	Gradual neurological, renal, and metabolic improvement. Vasopressor and ventilatory support successfully weaned
Day 10	Transferred from ICU to paediatric ward
Day 11-37	Continued renal recovery, physiotherapy, nutritional rehabilitation and multidisciplinary follow up
Day 37	Discharged home in stable condition with complete neurological recovery and improving renal function

ICU: Intensive care unit; DKA: Diabetic ketoacidosis.

DISCUSSION

DKA is a serious and potentially life-threatening complication of T1DM. Although cerebral oedema and AKI are recognized complications of severe pediatric DKA, the coexistence of cerebral oedema, recurrent seizures, dialysis-dependent AKI, haemodynamic instability, cardiac arrest, and prolonged mechanical ventilation with complete neurological and renal recovery remains uncommon, particularly in resource-limited setting[3]. The leading cause of death in DKA in children is cerebral edema, with 15%-35% of survivors facing permanent neurological deficits[4]. It has been reported that mortality in children with cerebral edema in developing countries was approximately 43%[4,5]. The risk factors for the development of cerebral edema in pediatric patients include severe acidosis, high urea nitrogen levels, and hypocapnia which was present in our patient[6].

The International Society for Paediatric and Adolescent Diabetes guidelines for management of cerebral edema in DKA emphasize immediate intervention with mannitol or hypertonic saline, reduced fluid rates, and elevating the head of the bed to 30°, focusing on preventing it through careful initial fluid management, but intervening aggressively once symptoms appear, as delaying treatment worsens outcome[7]. Our patient received mannitol in three doses, and hypertonic saline.

AKI is a common complication of DKA in children. In a study on children and adolescents with DKA at Kenyatta National Hospital in Kenya, Musoma et al[5] found that 15% of the children had elevated creatinine levels while 12% had reduced urine output. This finding was similar to that of Hamoodi et al[8] in Iraq who found an incidence of 19%. Other studies have, however, reported higher incidences ranging from 21.9%-80.2%[9]. Reported risk factors for AKI in these patients include clinical and laboratory characteristics that are associated with severe dehydration, such as increased heart rate, higher initial corrected sodium and blood urea, and lower serum bicarbonate[8,10,11]. Other risk factors include older age between 12 years and 14 years, higher body mass index, history of recurrent DKA, higher initial glucose levels, higher white blood cell counts above 15000 cells/mm³ and elevated neutrophil-lymphocyte ratio greater than 5.5[10-12].

In addition, Ahmed et al[9] found that delay in initiation of treatment, sepsis and low GCS score were risk factors for AKI among children with DKA. Our patient had several risk factors, including older age of 12 years, low GCS score, severe metabolic acidosis, high initial blood glucose level, and sepsis. These highlight the need for early identification of risk factors and preventive management strategies to avert the development of AKI and improve outcomes. Management of AKI includes fluid resuscitation, correction of electrolyte abnormalities and dysglycemia, and treatment of sepsis[13].

In terms of outcome, Musoma et al[5] found that children with high creatinine had a 5-fold higher risk of mortality compared to those with normal creatinine, while those with decreased urine output had a 9-fold higher risk of mortality. Ahmed et al[9] reported a high mortality rate of 84.5%.

The median duration of hospital stay and time to recovery of acidosis has been found to be longer among children with AKI compared to those without[10]. Bhowmick et al[14] found that 15% of patients had chronic kidney disease at the end of one year follow-up. This underscores the need for close follow-up of these patients to prevent progression to chronic kidney disease.

CONCLUSION

Early identification of acute complications, intensive monitoring, and appropriate multidisciplinary management is important in the management of DKA and helps in full recovery without any sequelae. This case underscores the importance of early recognition and prompt, guideline-based management of DKA to prevent morbidity and achieve favourable outcomes.