Case Study: Previously Healthy 16-Year-Old Girl Was Found Un

Case Studya Previously Healthy 16 Years Old Girl Was Found Unconscious

A previously healthy 16-year-old girl was found unconscious following a domestic argument. Upon examination, she was hyperventilating, responded to painful stimuli, and had dilated pupils that responded to light. The rest of her physical examination was unremarkable. Laboratory analysis revealed her urine was negative for glucose and ketones. The relevant laboratory values are as follows:

• Plasma sodium (Na): 141 mmol/L (reference range: 135-145)
• Plasma potassium (K): 3.4 mmol/L (3.2-4.8)
• Plasma chloride (Cl): 100 mmol/L (98-108)
• Plasma bicarbonate (HCO₃): 16 mmol/L (23-33)
• Blood urea: 6.5 mmol/L (3.0-8.0)
• Creatinine: 80 mmol/L (60-120)
• Anion gap: 25 mEq/L (6-16)
• Blood glucose: 5.5 mmol/L (3.5-5.5)
• Osmolality: 299 mmol/kg
• Total proteins: 70 g/L (63-80)
• Albumin: 43 g/L (32-50)
• ALT: 15 U/L (
• Total bilirubin: 12 μmol/L (
• Calcium: 1.86 mmol/L (2.15-2.55)
• Phosphate: 0.9 mmol/L (0.65-1.25)
• Blood pH: 7.45 (7.35-7.45)

Paper For Above instruction

The clinical presentation of this 16-year-old girl suggests a complex pathophysiological process that warrants a thorough interpretation of her laboratory results. Her initial signs—hyperventilation, altered consciousness, and dilated pupils—point to potential metabolic disturbances, neurological compromise, or intoxication. Her laboratory data reveal several key anomalies that help refine the differential diagnosis and point toward a specific metabolic disorder.

Her serum bicarbonate level is markedly decreased at 16 mmol/L, indicating a primary metabolic acidosis. Despite her hyperventilation, which is a compensatory response, her blood pH remains within the normal to slightly alkaline range of 7.45, reflecting the body's attempt to buffer and compensate for acid-base imbalance. The elevated anion gap of 25 mEq/L (normal 6-16) signals the presence of an unmeasured acid in her circulation—most likely an organic acid or ketone, although her urine tests are negative for ketones. The elevated serum osmolality of 299 mmol/kg suggests a degree of osmolar disturbance, potentially from the presence of toxic substances or dehydration.

One of the hallmarks here is the elevated anion gap metabolic acidosis with a low bicarbonate, which is characteristic of several conditions, including diabetic ketoacidosis, lactic acidosis, renal failure, ingestion of toxins such as methanol, ethylene glycol, salicylates, or the ingestion of certain toxins and drugs leading to acid accumulation. Her normal blood glucose reduces the likelihood of diabetic ketoacidosis. Renal function appears preserved given the normal serum urea and creatinine levels, making renal failure less likely as the primary cause.

Her hypocalcemia (serum calcium at 1.86 mmol/L) adds complexity. Hypocalcemia can be secondary to various causes, including metabolic acidosis, vitamin D deficiency, or intoxication with substances like ethylene glycol, which forms calcium oxalate crystals and causes hypocalcemia. The absence of significant hepatobiliary enzyme elevation and normal liver function tests suggests that her liver is not primarily affected.

Her clinical scenario—post domestic argument, hyperventilation, and altered consciousness—combined with lab findings such as high anion gap metabolic acidosis, hypocalcemia, low bicarbonate, and the clinical history of possible toxin exposure, suggests poisoning with substances like ethylene glycol or methanol. These toxins lead to an increased anion gap acidosis, with prominent metabolic disturbance and hypocalcemia due to calcium chelation by oxalate crystals or other metabolites.

Additionally, ethylene glycol poisoning presents with central nervous system depression, metabolic acidosis, calcium oxalate crystal formation, and renal damage. Although her urine does not show crystals, it is possible that early or insufficiently sensitive tests have missed crystals, or that her condition is in an early phase. The high osmolality might also point to the presence of toxic alcohols, which are metabolized into acids and oxalates, contributing to her clinical and laboratory picture.

In order to confirm this suspicion, further investigations are warranted. These include serum levels of ethylene glycol, methanol, and toxicology screening to detect ingested substances. Additionally, a blood gas analysis should be performed to precisely assess acid-base status, and urine microscopy may be useful to identify oxalate crystals or other abnormalities.

In conclusion, the most likely diagnosis in this case is ethylene glycol poisoning leading to high anion gap metabolic acidosis, hypocalcemia, and neurological symptoms. This diagnosis is supported by her clinical presentation, laboratory results, and the context of possible toxin exposure. Prompt recognition and treatment with fomepizole or ethanol (to inhibit alcohol dehydrogenase), correction of acid-base disturbances, and supportive care are critical in managing this potentially fatal condition.

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