NAC dosing requires adjustment during dialysis. Signs of altered mental status, metabolic acidosis, elevated lactate, and APAP>900 mg/L even if NAC is administered.Signs of altered mental status, metabolic acidosis, elevated lactate, and APAP>700mg/L and NAC is not administered.APAP >1000 mg/L and NAC not administered.Current EXTRIP guidelines recommend dialysis under the following circumstances Conventional protocols use the EXTRIP guidelines to determine dialysis needs. In massive overdose there may also be a role for intermittent hemodialysis (IHD) or continuous renal replacement therapy (CRRT). Further validation is necessary, but this work has provided rationale for current higher dose strategies. 6.25 mg/kg/h becomes 12.5 mg/kg/h, 18.75 mg/kg/h, or 25mg/kg/h depending on serum APAP concentration). This strategy effectively doubles, triples, or quadruples the final continuous infusion bag (i.e. al published a revised nomogram to help direct increased NAC dosing based on serum APAP concentrations. However, in massive overdose, an increased NAC dose may be necessary. Intravenous dosing typically involves a 150 mg/kl bolus over 60 min followed by 12.5 mg/kg/h for 4 hours (50 mg/kg over 4 hours) then 6.25 mg/kg rate (100 mg/kg over 16 hours). Acute ingestion standard NAC dosing can be given orally or intravenously. In an acute ingestion, the Rumack-Mathew Nomogram can be used to risk stratify patients and determine whether NAC is needed. A thorough history is crucial, however often difficult to obtain due to patients being unreliable (particularly those with suicidal ideations) or having altered mental status (as in our case). Traditional NAC dosing follows two specific treatment options which hinge on whether a reliable time of ingestion is known. Interestingly, methemoglobinemia is also a well-known side effect of APAP’s early ancestors phenacetin and acetanilide. Although a mechanism is unknown, it is hypothesized that this may be related to the oxidizing effects of the parent compound APAP or its metabolites. This has provided evidence to support increasing NAC dosing in these circumstances.Ĭase reports also describe methemoglobinemia in massive overdose. These massive overdoses produce a unique challenge in terms of management with case reports describing the occurrence of liver failure and death despite standard NAC treatment. In these instances, lactic acidosis and end organ failure may occur early in the APAP ingestion time course. Mitochondrial dysfunction is clinically seen with evidence of profound acidosis. In massive overdose, unchecked NAPQI levels lead to oxidative stress, mitochondrial dysfunction, and cell death. Regardless, massive overdose is a rare event. You fire off labs and they result below:ĪSA 30g to >50 g and massive APAP concentrations have been defined as >250 mcg/ml to >500 mcg/ml at 4 hours post ingestion. You decide to immediately intubate for airway protection. She has minimal bowel sounds and is hypo-reflexive. On arrival, you examine the patient and find her to be unresponsive to noxious stimuli, with pupils fixed at 4 mm bilaterally. Prior to Emergency Department (ED) arrival, she’s received 2 mg of naloxone with no effect. Emergency Medical Services (EMS) reports she was found in a parking garage unresponsive with an empty bottle of co-formulated acetaminophen/diphenhydramine (Tylenol PM). A 54 year old female presents to your emergency department via ambulance with chalky white residue around her mouth, hypotensive with a systolic blood pressure in the 80’s, and with a GCS of 4.
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