Page 625 - ACCCN's Critical Care Nursing

602 S P E C I A LT Y P R A C T I C E I N C R I T I C A L C A R E

Assessment, Monitoring and Diagnostics antipyretic agent. 109,124 The drug is absorbed in the
Intentional or accidental ingestion is straightforward, stomach and small bowel, with 98% metabolised by
with a clear history of poisoning. Chronic toxicity is the liver using one of two mechanisms: most by a
however often unrecognised. Individuals may not be pathway with breakdown into nontoxic byproducts;
aware of correct dosages, combine multiple drugs that the second hepatic pathway usually metabolises about
contain aspirin, or may have impaired excretion due to 4% of the drug, but the process has a toxic byproduct.
dehydration. The symptoms of chronic aspirin overdose The liver detoxifies this toxic byproduct by combining
(i.e. dehydration, lethargy, fever) resemble the original it with glutathione, a naturally-occurring substance. In
problem being treated, and some people will continue an overdose or when the minor pathway has already
treating themselves with aspirin for these symptoms. been stimulated (e.g. concomitant barbiturate use), more
Chronic toxicity has a higher mortality than acute paracetamol is metabolised by the secondary pathway
ingestion. 115,122,123 and the toxic byproduct accumulates, quickly consuming
the available glutathione, resulting in liver tissue
Aspirin is problematic if ingested in amounts greater than destruction. 109,124,126
150 mg/kg; toxicity presents with tachypnoea, fever, tin-
nitus, disorientation, coma and convulsions due to sys- Assessment, Monitoring and Diagnostics
temic effects of aspirin. 115,122,123 Acid–base disturbances
arise from direct stimulation on the respiratory centre in The amount of paracetamol ingested is best determined
the CNS; an increased rate and depth of respirations from patient history, as serum levels (although helpful)
cause hypocarbia and respiratory alkalosis, with renal can be easily distorted. A nomogram to plot measured
compensation by bicarbonate elimination. Salicylates, levels against time postingestion is a relative indicator
however, also alter metabolic processes, resulting in a of toxicity. A relatively small dose of 200 mg/kg
metabolic acidosis. Blood gases can therefore reflect aci- paracetamol is considered toxic, although hepatotoxicity
dosis, alkalosis or a combination. Tinnitus (ringing in the occurs after ingestion of 140 mg/kg or 10 g in a single
ears) is a symptom of the effect on the 8th cranial (acous- dose. 109,124,126
tic) nerve. 115,122,123 Liver function (liver enzymes, serum bilirubin, protein)
Aspirin also interferes with cellular glucose uptake, and coagulation tests (prothrombin time, partial throm-
causing initial hyperglycaemia. As cellular levels become boplastin time, platelets) identify the development of
depleted the patient demonstrates hypoglycaemic effects. hepatic dysfunction or damage. 109,124 The pattern of toxic
Later, serum levels may be either normal or hypoglycae- damage occurs over a characteristic three-phase course:
mic. 115,122,123 Patients may be nauseated and vomit after 1. First 24 hours: vague symptoms of nausea, vomit-
ingestion, causing fluid and electrolyte imbalance. 115,122,123 ing, and malaise.
Aspirin use is also associated with local tissue irritation, 2. 24–48 hours: above symptoms subside with onset
gastrointestinal bleeding, and platelet dysfunction, of right upper quadrant pain due to hepatic injury;
increasing risk of bleeding. Concomitant use of anti- urine output may decrease as paracetamol potenti-
coagulants therefore increases this risk. 115,122,123 ates the effect of antidiuretic hormone; liver
enzymes, bilirubin, proteins and clotting studies
Management may be abnormal.
Absorption can be reduced with activated charcoal, using 3. 60–72 hours: liver impairment becomes more
repeat doses for patients with signs of ongoing absorp- obvious, with jaundice, coagulation defects, hypo-
tion. 115,122,123 Urine alkalisation and forced diuresis can glycaemia and hepatic encephalopathy; renal
significantly increase elimination, as salicylates are weak failure or cardiomyopathy may also occur; death
acids excreted by the kidneys. 115,122,123 Haemodialysis from hepatic failure occurs in approximately 10%
is reserved for extreme cases with profound acidosis, of severe overdoses. 109,124-126
high blood levels, persistent CNS symptoms or renal
failure. 115,122,123 Management
As salicylates have no known specific antidote, 115,122,123 Absorption can be reduced with activated charcoal when
supportive therapy includes prevention of dehydration the patient presents to hospital early, however following
with careful monitoring of fluid output and adequate periods of 2 hours postingestion activated charcoal is
fluid replacement, monitoring serum electrolytes for unlikely to be effective. Haemodialysis with a charcoal
imbalance and replacement as needed. Evaluate ABGs to dialysate has been used to remove unchanged paracetamol
determine whether the patient continues to have meta- from the liver, but this does not remove the toxic
bolic effects from aspirin toxicity or is not responding to byproduct. Forced diuresis is also not effective, as
therapy. Control temperature elevations with external minimal paracetamol (about 2%) is removed by the
cooling methods if fever develops. kidneys. 126-128

Specific therapy is the use of an antidote, N-acetylcysteine,
PARACETAMOL POISONING which is structurally similar to glutathione and binds to
The incidence of paracetamol toxicity is associated with the toxic byproduct. When given within 24 hours of acute
approximately half of all Australasian toxic ingestions, ingestion, N-acetylcysteine is effective in preventing
due in part to its common availability as an analgesic/ hepatic damage. 126-128