EMERGENT INSIGHTS: ACUTE KIDNEY INJURY IN 7 MONTH OLD

Dr Joepaul Joy, Dr Vinitha Prasad, Dr Shela, Dr C Jayakumar
AIMS KOCHI 
KERALA 
INDIA 
 
Seven month old developmentally normal, immunized for age male child k/c/o Perimembranous VSD with Left to Right shunt restricted Septal Tricuspid Leaflet, Valvar PS, Doming pulmonary valve presented with complaints of vomiting since last 1 week, associated with greenish stools, 3-4 episodes per day. Was treated with Homeo medications for 3 days. Irrespective of management from alternative system of medicine and from near hospital stompers worsened one day back and brought to AIMS. 
Child was dehydrated with decreased urine output .But no h/o hematuria, cry while passing urine or altered sensorium. Diagnosis of ADD with severe dehydration was considered.
 
              At admission, child was febrile, sick looking with signs of severe dehydration- reduced skin turgor, depressed AF with dry oral mucosa. 
Systemic examination revealed Pansystolic murmur of grade 3/6 in the lower left parasternal border.
Labs done TC:23.40 k/uL 
CRP(22.8 mg/L)
Hemoglobins levels10.8 gm/dl
K+:5.4 mmol/L
Urea:48.2 mg/dl, 
Creatinine:1.67 mg/dl
Dehydration correction was given with Ringer lactate bolus and child was put on maintenance IV fluids. 
Repeat RFT 12 hrs later showed increase in blood urea (61.5 mg/dl) and serum Creatinine (3.11 mg/dl). 
VBG done showed metabolic acidosis(pH:7.29,HCO3-:14.1). Child was shifted to PICU 
Inj.Ceftriaxone was started adjusting the dosage in view of the high creatinine. 
In view of deranged RFT,IV fluids was changed to 5% dextrose. Strict input and output charting was kept. 
Chest Xray done was normal. 
USG Abdomen showed Bilateral kidneys are bulky and echogenic with tiny calculi/debris in left collecting system and Trace prominence of left collecting system.
Serum electrolytes repeated showed increasing K+ levels(6.1) 
Bicarbonate correction was given and antihyperkalemic measures were started. RFT repeated showed increasing trend of Urea and creatinine. 
He was diagnosed with AKI Stage 3. Peritoneal Dialysis was initiated. 
Eight cycles of Peritoneal dialysis were done. Regular RFT and ABG monitorings were done showed improvement. 
PT-INR was elevated(43.4/14.7/3.12) following which Inj.Vitamin-K was given. Daily urine output monitoring showed improvement. 
Child was slowly started on oral feeds. CBC,CRP repeated showed neutrophilic leucocytosis with increasing trend in CRP levels(83mg/L),following which antibiotics were escalated to Inj.Meropenem. Inj Vitamin-K was given for 5 days during which PT-INR levels checked showed improvement. Regular vitals monitoring done showed elevated BP readings following which oral Amlodipine was started. 
Serial CBC monitoring were done and showed low hemoglobin of 6.7 gm/dl following which 1 unit of PRBC transfusion was given. Blood and urine cultures were sterile. Repeat blood investigations showed improvement and antibiotic was deescalated to Inj Piptaz. In view of improving RFT and ABGs, PD was stopped and catheter was removed. Oral intake was improved and child was shifted back to the ward. Strict BP monitoring was done and Amlodipine was tapered and stopped. BP monitoring done was normal. Repeated blood counts, RFT showed improvement. Child improved with treatment given and discharged with stable vitals.
AKI is defined as the abrupt loss of kidney function that results in a decline in GFR, retention of urea and other nitrogenous waste products, and dysregulation of extracellular volume and electrolytes. It is classified as:
1. Prerenal AKI- due to decreased renal perfusion and is most commonly caused hypovolemia or decreased effective arterial perfusion due to heart failure, sepsis, or cirrhosis.
2. Intrinsic AKI- Due to injury to renal parenchyma and is most commonly caused prolonged hypoperfusion, sepsis, nephrotoxins, or severe glomerular diseases.
3. Postrenal AKI- This results from anatomic obstructions to the lower urinary tract.
Most children with AKI present with edema, reduce urine output, gross hematuria, and/or hypertension. Other children identified elevated serum creatinine as a result of ongoing monitoring in at-risk patients or as an unanticipated lab finding. Other lab findings at presentation include hyperkalemia, serum sodium abnormalities, metabolic acidosis, hypocalcemia and hypophosphatemia.
The diagnosis of pediatric AKI is made clinically based on signs and symptoms of kidney impairment as well as lab findings of kidney injury including an elevated or rising serum creatinine and/or abnormal urinalysis. Main differential diagnosis of AKI is an acute presentation of CKD.
Take home message: Appropriate and active intervention at right time in a case of AKI modify the outcome.