A 20 years old lady presented to ED 26 hours after ingesting 30 tablets of paracetamol after a fight with her family. On presentation she was complaining of mild epigastric pain and vomited twice . Clinically , she is conscious and alert , Vitals signs : pr; 90 , bp: 120/80 , RR: 20 , spo2: 99% in r.a , afebrile , blood sugar 6 mmol/l . , Rest of exam is unremarkable ,ECG and blood gases are normal
Your junior treated the patient symptomatically and she feels much better and acetaminophen level is shown
Q1 How you will proceed with this patient?
Q2 Your junior want to discharge this patient , what do you think?
Easy Pain Cont'
Excellent comments and discussion all, proud of you
This patient had elevated LFT on presentation which support her story of late presentation and she was treated on NAC course and she recovered from APAP induced hepatotoxicity despite late presentation.
Important points to pay attention to :
A negative APAP reading should not be interpreted alone / Should be with :
Time
Clinical context
Liver function test
2. Caution for use of Rumack- Mathew Normogram
Time coordinates refer to time post ingestion starting from 4-24 hrs
Graph relates only to plasma concentration following single acute overdose ingestion
3. Adult with intentional or suicidal ingestion are often unreliable , and you will need to verify the story if collateral history exist or take the worst case scenario
4.Acetaminophen toxicity goes into stages and this patient presented on stage 2 which could be mild symptoms( hence the easy pain could be deceiving ) but there will be rise in in LFT
5.Ingested dose of paracetamol alone is a poor risk assessment tool in accurately determining need for treatment with an antidote, so always send the level of paracetamol at 4 hours post ingestion if possible.
6. Liver damage is unlikely to occur if treatment is started within 8 of ingestion of a single overdose
7. One more pearl to remember , when in doubt to treat or not to treat with NAC, treat , and Consult Toxicologist 😉
References:
Rosen's 9TH edition
Goldfrank Toxicology
https://wikem.org/wiki/Acetaminophen_toxicity
And yes i forgot to add
Consult a toxicologist
A very nice case Dr.
In regard of APAP tox there are two options:
1) unreliable pt
Nausea and epigastric pain are signs of acute ingestion and should not to be taken lightly.
So she could have ingested the tabs prior to her presentation to ED as she attempt to harm her slef. So she is in STAGE 1 (sympoms mentioned above+normal labs and APAP level). If this is the case then i would go and repeat the test after 4 hours from her presentation.
Ofcourse make sure you send all the tox workup: coingestion, LFT VBG...etc.
2) pt is relaibale:
If she started to be symptomatic and The level is low then i will search for an organ damage.
That indicate the pt in advance stage of Toxicity (>stage 2).
For sure if she ingested the tablet she will have some kind of transiminitis , hyperbilirubinimia
Hypoglycemia, AKI ...etc
If the her labs are normal and no indicators of a secondary organ failure... i would think of another diagnosis rather than APAP tocicity.
Let’s summarize the case. A young adult lady presented with an intentional ingestion of 30 tablets ( ~ 15G ) of paracetamol, 26 hours ago. She is symptomatic with RUQ pain and repeated vomiting, otherwise stable at the moment with normalized serum apap level.
This is a delayed presentation of apap toxicity. Giving the potentially toxic amount of ingestion ( > 10g for adult ) with the symptoms, this lady presented in the second stage of apap toxicity where hepatic toxicity becomes evident especially when she was not started on NAC at the initial 8 hours post ingestion.
The delay presentation makes serum level of apap unreliable with the evidence of the actual toxicity. It won’t also be indicated to use the RM nomogram. Hence assessment of hepatic toxicity will depend on clinical and laboratory evaluation.
N acetyl cystine indicated ? Yes. Patient with hx of significant apap ingestion with symptoms suggestive of hepatic injury, to be supported by laboratory confirmation of hepatic injury, all of that indicates NAC administration regardless of the serum level or the delayed presentation.
Summery of management:
Continuous monitoring and ABC assessment
Send laboratory investigations to evaluate for hepatic injury and other organ injuries : Blood gas, CBC, full metabolic panel, U&R, LFT, coagulation profile, amylase.
Consider co-ingestion with other drugs E.g Aspirin.
Consult toxicology to start NAC ASAP.
Consult medicine as patient will need admission with monitored bed
Psychiatric assessment for intentional suicidal attempt.
Presentation varies according to stage of toxicity:
Stage 1 (0.5-24 hrs): mild nausea, emesis, weakness
Stage 2 (24-72 hrs): hepatotoxicity +/- nephrotoxicity => RUQ abdominal pain
Evaluate for co-ingestions: serum salicylate, serum ETOH; calculate an anion gap and an osmolar gap as appropriate. Consider UDS.
If ingestion spans more than 24 hours: Screen with labs (APAP concentration, hepatic function tests, renal function tests, coagulation studies, blood gas), assess patient risk factors and clinical features
If ASTs are elevated = treat with NAC
If APAP is detectable = treat with NAC
If APAP is undetectable and ASTs are normal = NAC is unnecessary
If lab testing shows progressive hepatic failure or continued detection of APAP = continue NAC (this implies repeat testing).
NAC is most effective if initiated within 8 hours of acetaminophen ingestion.
End point of NAC treatment: AST <100 U/L and acetaminophen <10mcg/mL or if extended therapy required: normalization of INR, resolution of encephalopathy, and decreasing AST (<1,000 U/L)
It is highly recommended to consult with a poison control center or medical toxicologist when considering the discontinuation of acetylcysteine prior to the conclusion of a full course of therapy.