Why won't you go get some antibiotics like I told you to?
Luckily for you, overdosing on Ibuprofen doesn't seem to have too many life threatening effects although you should definitely cut down on it. If Ibuprofen's not stopping the pain, then taking more won't help.
DOSING: ADULTS
Inflammatory disease: Oral: 400-800 mg/dose 3-4 times/day (maximum: 3.2 g/day)
Analgesia/pain/fever/dysmenorrhea: Oral: 200-400 mg/dose every 4-6 hours (maximum daily dose: 1.2 g, unless directed by physician)
OTC labeling (analgesic, antipyretic): Oral: 200 mg every 4-6 hours as needed (maximum: 1200 mg/24 hours)
Overdosage effects:
LINICAL ASPECTS OF ACUTE TOXICITY
General — Acute toxic ingestion of NSAIDs often present to emergency departments and represent a sizable percentage of cases reported to regional poison centers [1] . The clinical manifestations of acute NSAID overdose tend to be minimal. In a review of over 5000 NSAID overdoses, the most common signs and symptoms were nausea, vomiting, drowsiness, blurred vision, and dizziness [8] . Less than 0.5 percent of these patients experienced severe harm (eg, renal failure); most required no medical intervention. In general, ingestions of less than 100 mg/kg of most NSAIDs (except mefenamic acid and phenylbutazone) are unlikely to cause any significant toxicity. Massive ingestions with severe symptomology are seen with ingestions greater than 400 mg/kg [9] .
Acid base abnormalities — An increased anion gap metabolic acidosis may be seen after large ingestions of NSAIDs, particularly ibuprofen, naproxen, and phenylbutazone (a veterinary NSAID occasionally ingested by humans). This acidosis may represent a combination of lactic acidosis (from cellular hypoxia or seizures) and weakly acidic NSAID metabolites.
Renal insufficiency and renal failure — Acute forms of renal failure and renal papillary necrosis are rare in NSAID overdose. Most commonly, these pathologic processes occur in patients with decreased effective arterial volume (congestive heart failure, cirrhosis, protracted dehydration), age-related underlying renal dysfunction, or massive overdose.
Patients with NSAID-induced acute renal failure usually present with evidence of decreasing renal function (increased BUN, increased creatinine, hyperkalemia, decreased urine volume, or weight gain).
The diagnosis of acute renal papillary necrosis may be more difficult. Patients classically present with gross hematuria and renal colic, secondary to ureteral passage of sluffed ischemic renal tissue. Often the clinician must inquire specifically about a recent large ingestion of NSAIDs to confirm the diagnosis. (See "Manifestations and diagnosis of analgesic nephropathy").
NSAID-induced renal injury likely results from inhibition of vasodilatory prostaglandins. Prostaglandins preferentially dilate efferent arterioles in the glomerulus, helping to maintain renal perfusion; prostaglandin inhibition shifts the balance towards vasoconstriction and decreased perfusion. Discontinuation of NSAID use has been shown to reverse the renal insult in most cases [10-14] .
Central nervous system toxicity — Acute central nervous system toxicity related to NSAID use is pervasive and varied. A prospective study looking at ibuprofen overdose noted that 30 percent of patients experienced CNS effects ranging from drowsiness to coma [7] . Case reports have identified numerous neurologic sequelae including ataxia, nystagmus, headaches, and disorientation [15] .
Seizures have been reported with ingestions of propionic acids (ibuprofen), pyrazolones (phenylbutazone), acetic acids (diclofenac and indomethacin), and anthranilic acids (mefenamic acid and meclofenamate) [16-21] . Most cases occurred after large ingestions, but even small therapeutic doses have been associated with seizures in certain patients. The mechanism by which NSAIDs cause seizures is not clear. Some speculate that decreased cerebral prostaglandin and thromboxane synthesis may lower the seizure threshold [19,21] . Seizures are effectively treated with benzodiazepines.
Hematological toxicity — Aplastic anemia and agranulocytosis have been associated with the use of phenylbutazone and indomethacin [22,23] . In one case of aplastic anemia, the patient presented with bleeding gums and a diffuse petechial rash after ingestion of an herbal supplement containing phenylbutazone [23] . Phenylbutazones were removed from US markets in the 1970s, but they are still available in veterinary formulations and in other countries. Discontinuation of the drug has been shown to reverse the hematologic disturbances.
Allergic reactions — NSAIDs may cause anaphylactic and anaphylactoid reactions, particularly in patients with chronic urticaria or asthma [24] . This is due in large part to cyclooxygenase-1 (COX-1) inhibition and resultant overproduction of leukotrienes [25,26] (show figure 1). Patients may present with any degree of severity, from mild urticaria and rash to hypotension and cardiac arrest. Standard treatment for anaphylaxis is effective. (See "Anaphylaxis: Rapid recognition and treatment", section on Management). All patients with NSAID or aspirin-related allergies should discontinue all nonsteroidal medications, due to unknown rates of cross reactivity.
The safety of COX-2 inhibitors in patients with known NSAID allergies is unclear. Four reported cases of adverse reactions to celecoxib suggestive of anaphylactic shock have been reported [27] . Due to the paucity of data regarding safety, current recommendations are that patients with known NSAID allergies should refrain from using COX-2 inhibitors.
