A 3-Year-Old Nearly Died From a Paracetamol Dosing Error in Kenya — and It Almost Happened Twice

Paracetamol is one of the most trusted medicines in the world, a drug so familiar that it sits in kitchen cabinets on every continent and is given to children without a second thought. But a case report from coastal Kenya, published in the journal Discover Toxicology, shows how easily that trust can be shattered when a single prescription error collides with a fragile healthcare system. A previously healthy three-year-old girl from Kilifi County received a cumulative dose of 5000 milligrams of paracetamol over just three days — nearly triple the therapeutic dose appropriate for her 10-kilogram body weight — and came within hours of fatal liver failure before clinicians finally pieced together what had happened.

The story began on 31 May 2023, when the girl’s grandmother brought her to a local health center with cough, runny nose, and fever. She was discharged with amoxicillin dispersible tablets, cetirizine syrup, and paracetamol tablets. What followed was a cascade of miscommunication. The prescription itself was barely legible and omitted critical details — the patient’s name, her age, and even the prescriber’s identity — making it impossible to tell whether the medication was intended for the child or the grandmother. The dispensing envelope the grandmother received simply abbreviated the drug as PCM, and she administered the tablets exactly as she understood the label: 1000 milligrams on the first day, 3000 milligrams on the second, and another 1000 milligrams on the third. The correct total for a child her age would have been roughly 1800 milligrams across the entire period.

Within days, the child’s condition deteriorated dramatically. A private facility diagnosed gastroenteritis and prescribed cotrimoxazole and promethazine, missing the true cause entirely. By 4 June, she arrived at Malindi Sub County Hospital with severe dehydration — sunken eyes, skin pinch lasting more than two seconds, reduced skin turgor — along with pneumonia, evidenced by crepitations and rapid breathing. She received aggressive rehydration with Ringer’s lactate, multiple antibiotics, and zinc supplementation. Then, at 5:30 in the evening, she began to convulse, requiring an intramuscular loading dose of phenobarbital. Even at this point, paracetamol poisoning was not on the diagnostic radar.

The turning point came the next morning, when clinicians took a more detailed history and asked the grandmother to present every medication given before admission. Medication reconciliation — the systematic process of comparing what a patient actually took against what was prescribed — revealed the overdose immediately. Liver function tests confirmed the suspicion with striking clarity: alanine aminotransferase peaked at 1566.2 IU/L, far above the 1000 IU/L threshold conventionally used to define hepatotoxicity, while aspartate aminotransferase reached 302.3 IU/L. Gamma-glutamyl transferase climbed steadily and albumin fell, painting a biochemical picture of an injured liver. The ALT-predominant pattern, with the two transaminases rising in near 1:1 proportion, is characteristic of paracetamol-induced liver injury and helped distinguish it from other causes of hepatic damage.

Then the resource limitations of the setting began to bite. Malindi Sub County Hospital did not stock N-acetylcysteine, the antidote that replenishes glutathione and neutralizes the toxic metabolite NAPQI responsible for paracetamol’s liver damage. Serum paracetamol levels, prothrombin time, and international normalized ratio — the standard laboratory tools for assessing poisoning severity and coagulation status — were simply unavailable. When clinicians attempted to place a nasogastric tube, the child’s nose began to bleed; oozing also appeared at her intravenous cannula site. These clinical signs of coagulopathy, combined with hypoalbuminemia, forced the team to act empirically, administering vitamin K and fresh frozen plasma without laboratory confirmation, a pragmatic departure from guidelines that caution against routine plasma use in pediatric liver failure.

Sourcing the antidote became an ordeal in itself. The nearest supply of N-acetylcysteine was 232 kilometers away in Mombasa, and the pharmacy there would only sell an entire pack of ten ampoules when the child needed just two or three. The family lacked coverage from the National Hospital Insurance Fund, Kenya’s universal health insurance scheme at the time, and the cost was beyond their means. Only when a well-wisher stepped in to pay was the antidote secured. The first infusion began at 9:00 pm on 6 June — roughly 80 hours after the last paracetamol dose, far beyond the traditional window in which the antidote is considered most effective.

What happened next surprised the clinical team. Despite the delay of more than 84 hours from initial exposure, the child’s liver enzymes began to fall rapidly after N-acetylcysteine therapy, with ALT dropping to 431.1 IU/L and AST to 105.6 IU/L within days. Several hours into the third infusion, she regained consciousness, fully oriented, with a Glasgow Coma Scale score of 15/15 and stable vital signs. She received fresh frozen plasma on alternate days to guard against hemorrhagic complications, along with supportive care including dextrose infusions, vitamins, and lactulose. By 14 June 2023, just ten days after the overdose began, she was discharged having made a full recovery.

The case, the authors argue, is less a story of individual negligence than of compounding system failures. Incomplete prescriptions and careless dispensing practices are well-documented drivers of medication errors, particularly when drugs are handed over without patient-specific information. Caregiver misunderstanding and poor communication compound the risk, especially when health literacy is low and the dispensed formulation — adult tablets, in this case — is inherently unsuitable for a toddler. Research has suggested that standardized dosing instruments, metric-unit labeling, and picture-based dosing instructions could substantially reduce these administration errors. The diagnostic delay also reflects a broader pattern: early paracetamol poisoning mimics common childhood illnesses like gastroenteritis, with vomiting and lethargy masking the underlying toxicity until the liver begins to fail.

The authors also emphasize a lesson that may resonate far beyond Kenya: even when N-acetylcysteine is given very late — more than 24 hours after exposure — it can still abrogate severe hepatotoxicity in children. This finding challenges the rigid therapeutic windows that dominate high-resource guidelines and offers hope for clinicians working where delayed presentation is the norm rather than the exception. At the same time, the case exposes uncomfortable truths about access to essential medicines in low- and middle-income countries, where antidote stockouts, bureaucratic procurement barriers, and absent insurance coverage can force families to depend on charity for life-saving treatment. The authors call on prescribers to write complete, legible prescriptions; on pharmacists to communicate clearly with caregivers of all literacy levels; and on hospital administrators to encourage enrollment in government-subsidized health coverage.

As a single-center case report, the account cannot be generalized to every setting, and the authors acknowledge this limitation candidly. Yet its value lies precisely in the detail: a near-legible prescription, a dispensing envelope, a grandmother doing her best with the information she was given, a hospital pharmacy without the antidote, and a 232-kilometer journey that stood between a child and survival. Paracetamol was first synthesized in 1878 and marketed in 1955, and its overdose potential was recognized soon after it reached the market. Half a century of research — from the glutathione-dependent mechanism of toxicity elucidated in the 1970s to the Rumack-Matthew nomogram and the Prescott protocol — has made paracetamol poisoning one of the most treatable toxicological emergencies in medicine. This Kenyan case is a reminder that the science is settled; what remains unfinished is the harder work of ensuring that the systems around the medicine, from the prescription pad to the pharmacy shelf, are built to protect the children who depend on them.

Subject of Research: Pediatric paracetamol poisoning caused by medication error and managed in a resource-limited Kenyan hospital

Article Title: A cautionary tale of pediatric paracetamol poisoning in a low-resource setting in Kenya: a case report and review of the literature

Article References: A cautionary tale of pediatric paracetamol poisoning in a low-resource setting in Kenya: a case report and review of the literature. (n.d.). https://doi.org/10.1007/s44339-026-00047-z

Image Credits: AI Generated

DOI: 10.1007/s44339-026-00047-z

Keywords: paracetamol, acetaminophen overdose, N-acetylcysteine, hepatotoxicity, pediatric poisoning, medication error, Kenya, resource-limited setting, liver function tests, coagulopathy, medication reconciliation, case report