Poisoning is one of the common causes of self-harm. In rural areas, exposure to plants and their effects is responsible for a large number of unknown fatalities, especially in Africa. Adenia ellenbeckii is a monoecious shrub that grows primarily in the desert and tropical regions. The fruits of this plant are bright orange-red when ripe, and its decoction is used for treating wounds. It has also been mixed with meat to poison hyenas. It’s rarely ingested by humans. We hereby report a case of four siblings who unintentionally ingested the fruits of the plant in the rural area of the east Togdheer region in northern Somaliland, one of whom progressed to acute kidney injury with a fatal outcome. To the best of our knowledge, this is the first case report of acute kidney injury due to poisoning with Adenia ellenbeckii.
Introduction
Acute kidney injury caused by toxic substances has epidemiological different causes associated with cultural differences, tropical diversity, and socioeconomic status [1]. According to a 10‐year retrospective study of forensic autopsy cases in China, poisonous plants are thought to be the cause of up to 7% of poisoning deaths [2]. In Africa, herbal remedies increase morbidity and mortality rates, despite the fact the causes are frequently underestimated [3]. Children are more prone to such poisoning. In Botswana and South Africa, children under the age of 20 years account for approximately 60% of all acute poisonings [4]. A report from Nigeria previously revealed on acute toxic nephropathy that Anuria was a prominent feature occurring in 9 (90%) of their study participants were (33.3%) ARF had toxins responsible for their renal failure [5]. while PD is frequently used in young children with AKI, in this circumstance the only possible option was HD. Although hemodialysis is the most frequently used ECR of poisoned patients receiving extracorporeal treatments for enhanced toxin elimination in pediatrics and adolescents. [6]. These highly poisonous Adenia plants, which are publicly sold, represent a danger to anyone handling them, particularly children. Perhaps the worst aspect is that native or recombinant plant parts or their toxins could be exploited for bioterrorism, conflict, or even criminal activity, as it is feared for ricin [7, 8]. In recent years, the availability of such products has increased as a result of widespread internet use [9]. this is the first case report of acute kidney injury due to poisoning with Adenia ellenbeckii.
Case Presentation
A 4-year-old female child and her three siblings were referred to our hospital emergency department due to generalized body swelling, mainly in the lower extremities bilaterally, and anuria for 12 hours. The children were all healthy six days prior to their admission to the hospital and had no additional known complaints or symptoms. However, the patient's parents acknowledged that she and three of her siblings ingested the fruits of a poisonous plant known as Adenia ellenbeckii and brought some of the plant's fruits home to share with the rest of their cousins. They all became severely ill on the exact same night, developing a fever, sweating, frequent vomiting, and itching. All of the siblings had a significant history of ingesting Adenia ellenbeckii's fruits.
They were taken to a nearby hospital and managed initially and then referred to our hospital in view of the above-mentioned symptoms and worsening kidney function with generalized weakness. On examination, the child was febrile and averagely nourished. Her temperature was 38.2 °C, with a blood pressure of 78/50 mmHg, a pulse of 90 beats per minute, and an oxygen saturation of 92% on room air. Her lungs were clear to auscultation and percussion. Her cardiac rate and rhythm were regular, and there were no cardiac murmurs. Her abdomen was soft and non-tender to palpation, and neurological examination was unremarkable.
Blood tests on 1st hospital day showed abnormal kidney function with a serum creatinine of 5.83 mg/dL and urea of 108.5 mg/dL, hypokalemia, and hypoglycemia. Her hemoglobin level was 9.1 g/dL, and her white blood cell count was 57.33 x 109/. Urine analysis showed microscopic hematuria and proteinuria. A chest x-ray and abdominal ultrasound were unremarkable. Lab parameters during the hospital course are mentioned in Table 1.
A diagnosis of acute kidney injury due to poisoning was made and the patient was started on Ceftriaxone at 500 mg/kg/dose every 12 h, Ciprofloxacin 20 mg/kg/day, maintenance IV fluids, and furosemide injections of 10 mg every 12 h, paracetamol infusion (PRN), and Ondansetron 2 mg every 24 h. The acute kidney injury was initially attributed to systemic inflammatory response syndrome and possibly to acute tubule-interstitial nephritis related to the plant as the kidney biopsy could not be done due to the unavailability of kidney biopsy and the poor general condition of the patient. The patient showed no signs of kidney function recovery on the 2nd day of hospitalization. The patient had to be dialyzed after placing a double-lumen 8-Fr femoral venous catheter. The patient’s condition continued to deteriorate despite dialysis, and she was transferred to the pediatric ICU. She had persistent coagulopathy, fever, tachycardia, hypotension, and increasing inotropic requirements on the 3rd day of hospitalization. Unfortunately, the patient didn’t respond well to the treatment and passed away on the 3rd day of the hospital stay. The second child had a similar scenario in terms of renal function. He developed AKI similar to the first child. However, he responded well to treatment, and his kidney function completely normalized, following which After being discharged from the hospital, he was taken to a neighboring country for additional check-ups. The third and fourth children had normal kidney function except for showing abnormalities in their full blood count laboratory results. They were discharged from the hospital, therefore indicating that perhaps the effects of the plant might vary depending on the ingested quantity.