Immunology/ toxicology Flashcards
- State 4 mechanisms for the development of anaphylaxis - provide examples of each
- List 5 risk factors that increase the risk of death from an anaphylactic reaction
- What classification system is used for immune reactions?
Complete the table
- Regarding the recognition of anaphylaxis in ED complete the table below:
Immunological
-Type I hypersensitivity: IgE mediated mast cell granulation e.g. penicillin
Non IgE mediated mast cell activation
-Direct mast cell degranulation
-e.g. Contrast reaction
Immune complex mediated
-Whole blood (transfusion reaction)
Physical anaphylaxis
-Exercise, cold
Extremes of age (very young, elderly)
Comorbid conditions
-Cardiovascular disease
-Pulmonary disease (asthma, COPD, acute infection)
Use of Beta blockers and ACEI
Alcohol
Recent episode of anaphylaxis
An anxious 64 year old woman presents to the Emergency Department with a one hour history of acute onset swollen tongue and lips. She is drooling. There has been no trauma. She can speak though it is difficult to understand her. She has no stridor.
She has a past medical history of hypertension for which she takes hydrochlorothiazide, enalapril and nifedipine controlled release
Her observations are:
-Temperature: 36
-Pulse: 100
-Blood pressure: 180/100
-RR: 20
-Sats 98% on RA
- List 4 diagnoses that most likely match this woman’s symptoms
- Prescribe 3 empiric drug treatments in the drug chart below you would consider in this woman, giving your dose, route of administration for each
- Give 3 criteria that would lead you to consider short stay unit as your disposition pathway from the ED
Angioedema without urticaria (bradykinin mediated)
ACEI / NSAID related angioedema
-Usually within 1-2 weeks of starting ACEI
Hereditary angioedema
-Presents in childhood
-Type I C1 esterase deficiency
-Type II decreased function
-Minor trauma precipitates angioedema
-Decreased quantity or activity of C1 esterase inhibitor
-Low C4 is screening test
Acquired angioedema
-> 40 years old
-Paraneoplastic consumption of C1 esterase inhibitor, autoimmune antibodies against C1 esterase inhibitor
-Low C4 is a screening test
Treat acquired and hereditary angioedema with Icatibant (inhibits bradykinin receptors) 30mg subcut
TPA associated angioedema
-While TPA being administered or shortly after
Idiopathic angioedema
Local condition
-Ludwig’s angina
Angioedema with urticaria (IgE, histamine mediated)
Anaphylaxis
-Serum tryptase (within 3 hours)
-Treat with adrenaline 0.5mg IM, repeat every 5 mins up to 3 doses
-Adrenaline infusion commencing at 0.05mcg/kg/min
-On beta blockers give glucagon 1mg IV
-Steroids to reduce incidence and severity of biphasic reactions
-C1 esterase inhibitor concentrate (Berinert) 20IU/kg IV
-Icatibant 30mg subcut
-Adrenaline 0.5mg IM
-Need to respond to treatment
-Problem expected to resolve within 12-24 hours
-Concern for airway compromise so not suitable candidate
-Not appropriately staffed obs unit
A 5 year old girl presents to ED with swelling of the face as shown in the picture.
- List 10 important conditions to consider in the differential diagnosis of anaphylaxis
- State the criteria for diagnosing anaphylaxis
Further history reveals that she had a sudden onset of shortness of breath and facial swelling 30 mins ago. She has no known PMH and recently was treated for a ‘flu like illness’ at her GP
Her vital signs are as follows:
HR: 155
CRT: 3s
BP: 80/44
RR: 30
Sats: 90% on RA
- List your escalating management steps for this child
What specific causes of her presentation would you ask about on history?
In the context of managing anaphylaxis how would the following affect your management:
a. Refractory hypotension
b. Patient on regular beta blockade
Anaphylaxis differential diagnosis
Shock differential diagnosis
Upper airway disorders
-Epiglottitis, Ludwigs angina, quinsy, FB aspiration
Status asthmaticus
PE
Causes of oedema
-Angioedema - hereditary / acquired
-Renal disease - nephrotic syndrome
-Liver disease
-Protein losing enteropathy
-SVC obstrction
Causes redness or urticaria
-Flush syndrome (alcohol, scromboidosis)
-Carcinoid syndrome
-Phaeocrhomocytoma
-Mastocytosis
-Red man syndrome (vancomycin)
Anaphylaxis highly likely when any one of the following three criteria is fulfilled:
- Acute onset of illness with involvement of skin, mucosal tissue or both (e.g. hives, pruritis, flushing, swollen lips-tongue-uvula) and at least one of the following
a. Respiratory compromise (SOB, wheeze, stridor, hypoxia)
b. Reduced BP or associated symptoms of end organ dysfunction (hypotension, collapse, syncope)
- Two or more of the following occuring rapidly after exposure to a likely allergen for that patient
a. Involvement of the skin-mucosal tissue (hives, itch-flush, swollen lips-tongue-uvula)
b. Respiratory compromise (e.g. dyspnoea, wheeze, stridor, hypoxia)
c. Reduced BP or associated symptoms
d. Persistent GI symptoms (abdominal pain, cramping vomiting)
- Reduced BP after exposure to a known allergen for that patient
a. Infants and children low SBP
-Low systolic blood pressure for children is defined as <70 mm Hg from 1 month to 1 year old, <70 mm Hg + (2 × age) from 1 to 10 years old, and <90 mm Hg from 11 to 17 years old
b. Adults: SBP < 90
2.
-Remove trigger, trendelenburg position
-IM adrenaline 0.01ml/kg of 1:1000 = 10mcg/kg dose every 5 mins aiming for improvement in facial swelling, sats > 94%, RR < 25, SBP > 80, HR < 120, CRT of 2s
-Oxygen via NRBM (15L/min) aiming sats > 94%
-IV/IO access and fluid bolus 20ml/kg
-IV adrenaline infusion commencing at 0.05mcg/kg/min if unresponsive to initial treatment or required 3 IM doses
-If develops stridor nebulised adrenaline 5mg every 10 mins
-If wheeze nebulised salbutamol 5mg
-Hydrocortisone 4mg/kg IV or prednisolone 1mg/kg
a. Adrenaline infusion commencing at 0.05mcg/kg/min, noradrenaline infusion commencing at 0.05mcg/kg/min, ECMO
b. Glucagon 0.5mg (<25kg) to 1mg (>25Kg) IV, transcutaneous pacing if bradycardia, atropine 20mcg/kg if bradycardia
A 20 year old man presents to ED with significant facial swelling and pain in the affected parts. He describes a gradual onset over 3 hours. He recently recovered from a shoulder injury. His vital signs are normal and he does not have any rashes, respiratory or cardiovascular symptoms or signs
- List 6 possible causes for his appearance
- What further testing does the patient need?
Drug induced angioedema - NSAIDs
Hereditary angioedema
Acquired angioedema secondary to autoimmune deficiency or paraneoplastic syndrome
Infection
Anaphylaxis
-C4 level
-C1 esterase inhibitor levels and function
-Serum tryptase
-In adults administer Icatibant 30mg subcutaneously or C1 esterase inhibitor concentrate (Berinert) 20 units/kg IV
-In children use berinert 20IU/kg
Additional hospital treatment
-IV rehydration
-Opioid analgesia
-Second dose of specific treatment if inadequate response after one hour
-Emergency intubation or cricothyrotomy
A 55 year old man presents to ED complaining of swelling of his face. He was recently diagnosed with sinusitis and was treated with amoxicillin for 10 days. His last dose was 2 weeks ago. He was also treated with ibuprofen which he continues to take for pain. He also has a background history of hypertension and angina and is on ramipril and aspirin daily for this. His appearance is shown:
- What conditions need to be considered in his differential diagnosis? Complete the table below with 5 important conditions, stating 5 important clinical features on history and examination that would represent that condition. List the important investigations required or the diagnostic strategy to confirm the condition and the key management components required for each condition.
- You decide the patient needs antibiotics for severe facial cellulitis with features of sepsis. The patient states his mother told him about a reaction to penicillin when he was a child. You are concerned about possible penicillin allergy.
State 6 possible adverse reactions one can get from penicillin. Do not include conditions included in question 1. For each condition state 3 important clinical features for each condition. State the potential investigations required to suggest or confirm the diagnosis or the diagnostic strategy required
- State the management approach for each of these potential reactions (based on past history) when needing to consider antibiotic therapy for this mans infection
1/2. See table
Avoid penicillin, cephalosporin or carbapenem
-Type I IgE mediated reaction
-DRESS
-SJS/TEN
Can use penicillin but consider alternative
-Delayed reaction
A 74 year old man with ischaemic heart disease, CCF and COPD was swimming in a shallow rock pool at a popular beach on the tropical north coast of Australia. He is unsure if he felt a bite or a sting on his foot or leg while wading in the rock pool, but became anxious, nauseated and agitated. His wife escorted him out of the water and brought him to your ED which is a short 5 minute drive from the beach.
- State 6 relevant toxicological differential diagnoses to consider
- For each condition state 3 key clinical features to help differentiate the condition
- State the management required for each condition
Irukanji Syndrome
-Jelly fish found in costal waters of tropical Australia
-Can cause a severe pain syndrome, life threatening hypertension, cardiomyopathy, pulmonary oedema
-Toxin causes massive catecholamine release
-Initial sting not felt, no local signs are minimal or absent
-Systemic symptoms develop 30-120 mins after sting
-Agitation, vomiting, sweating, severe pain in back, limbs or abdomen, hypertension and tachycardia
-Potentially life threatening emergency
Treatment
-IV fentanyl until adequate analgesia achieved
-Severe hypertension refractory to opioid treated with IV GTN to achieve SBP < 160, alternative labetalol
-Nausea and vomiting can be treated with droperidol
-No antivenom
-Symptoms resolve after 12 hours
Blue ringed octopus
-Found in shallow costal waters around Australia
-Envenoming causes rapid paralysis
-Timely support of airway and ventilation ensures a good outcome
-Potent sodium channel neurotoxin
-Bite may not be painful
-Local symptoms often minimal or absent
-Rapid progress symmetrical descending flaccid paralysis manifests within minutes
-Early signs include ptosis, blurred vision, diplopia and difficulty swallowing. In severe cases, generalised paralysis, respiratory failure and hypoxic cardiac arrest ensure
-With appropriate support paralysis spontaneously resolves in 1-2 days
Management
-Pressure bandage with immobilisation prehospital
-If respiratory failure need intubation and ventilation
-No antivenom
Sea snake
-Toxin contains neurotoxins and myotoxins
-Most bites are small, relatively painless and not associated with local swelling or lymphadenitis
-Non specific features of envenoming include headache, nausea, vomiting and abdominal pain
-Systemic features of neurotoxicity and myotoxicity may become clinically apparent after a delay of severe hours
-Neurotoxicity: symmetrical descending flaccid paralysis. Early signs include ptosis, blurred vision, diplopia and difficulty swallowing. Can progress to generalised paralysis and respiratory failure.
-Myotoxicity: diffuse myalgias and myoglobinuria may progress to renal failure
Management
-Apply pressure bandage
-If respiratory failure occurs, intubation and ventilation
-Sea snake antivenom is the specific treatment of envenoming, give 1 ampoule
-Test FBC, CK, coagulation studies, D-dimer
-Severe envonomings can lead to CK levels > 100, 000
Box Jellyfish
-Causes immediate pain
-Found in tropical Australian waters.
-Most stings are benign and require only symptomatic treatment
-Severe envenoming can cause death within minutes of the sting secondary to cardiac toxicity
-Immediate CPR provides best chance of survival
-Toxin causes intracellular calcium accumulation in myocardial cells –> tetanic contraction and arrest
-Stings are associated with severe pain, typically lasting up to 8 hours.
-Linear welts in a cross-hatched pattern
-30% of cases tentacles are still adherent
-Hypertension, tachycardia, dysrhythmias
Management
-Apply vinegar to visible sting then remove adherent tentacles, wash sting with sea water
-Ice packs for pain management
-Do not apply pressure bandage with immobilisation
-Administer box jellyfish antivenom 1-3 ampoules over 5-10 minutes for cardiorespiratory arrest or shock (not for pain)
Blue bottle Jelly fish
-Ubiquitous in Australian coastal waters and stings frequently
-Stings cause immediate burning pain lasting up to 2 hours and linear erythematous welts
-Non specific symptoms such as headache, nausea or malaise may occur
Management
-Mild self limiting
-Hot shower for 20 mins
-Oral analgesics
-No pressure bandage
-No antivenom
Stone Fish
-Reef fish found in waters of Northern Australia
-Toxin contains vascular permeability factors, tissue necrosis factors and a vasodilator
-Causes immediate severe pain at sting site
-Local swelling, bruising and puncture marks
-Remnants of spine may be left in the wound
-Systemic envenomation rate
-Non specific features include nausea, vomiting, dizziness and dyspnoea
Management
-Immerse both limbs in hot water
-Supportive treatment
-Continue hot water immersion
-IV opioids
-Consider regional anaesthesia with local acting local anaesthetic
-If refractory to hot water immersion, opioid analgesia and nerve block then give 1 ampoule of antivenom for every to puncture wounds (maximum of 3 ampoules)
-Plain XR or US may detect retained FB
Sympathomimetic like syndrome
-Irukanji Syndrome - minor sting, delayed onset, opioids, GTN, droperidol
-Box jellyfish - immediate pain, vinegar –> remove stings, 1-3 ampoules of antivenom if cardiorespiratory arrest or shock
You are working as the doctor on a helicopter retrieval service that is dispatched to retrieve a 50 year old patient that has collapsed on a dive boat from a tour company. The patient has a history of asthma and hypertension.
- List 8 key aspects on the focused dive history to ascertain; provide a reason for each aspect
- List 6 important non-dive related differentials that need to be considered
- For each of the following categories, list 2 conditions associated with the mechanism of injury and provide 3 descriptive details for each condition
- Disorders related to descent
- Disorders arising at depth
- Disorders arising on ascent
- What transport related considerations are important?
-Number of dives and ascents
-Depth of dive
-Time spent at bottom
-Decompression or safety stops performed
-Which gases used in SCUBA apparatus
-Timing of collapse in relation to resurfacing (AGE vs DCS)
-PMH (cardiac, seizures)
-Medications
-Patten of symptoms (barotrauma vs AGE vs decompression illness)
ACS
Dysrhythmia
PE
Aortic dissection
ICH - SAH
Trauma - SDH
Envenomation - sea snake bite
Conditions on descent
-Middle (tinnitus, vertigo) and inner ear barotrauma (vertigo, tinnitus, hearing loss, vomiting)
-Barosinusitis (facial pain, epistaxis)
Conditions at depth
-Nitrogen narcosis - ‘drunk’ behaviour, treatment is ascending
-Oxygen toxicity - if using > 20% oxygen - muscle twitching, seizures, vision changes
Conditions on ascent
Decompression sickness - usually presents within 3 hours - can be delayed up to 24 hours
-Most common is type I - ‘the bends’ –> joint pain, rash
-Type II causes neurologic / pulmonary symptoms, more severe, patchy spinal cord findings, treat with IV fluid, oxygen, hyperbaric oxygen therapy
-Arterial gas embolism - air bubbles forced into pulmonary veins –> systemic circulation - symptoms within 10 min of surfacing - IV fluid, oxygen, hyperbaric oxygen therapy - may have PFO
–> MI, stroke etc.
-Pulmonary barotrauma –> pneumomediastinum, pneumothorax - symptoms can be delayed several hours
4.
-Fly at low altitude
-If arterial gas embolism needs to lie flat
-Need 100% high flow oxygen
-Need urgent hyperbaric chamber
What disorders benefit from recompression therapy?
Decompression sickness type I
Decompression sickness type II
Arterial gas embolism
You are notified about a 23 year old female enroute to ED via ambulance with an altered level of consciousness and a history of 10 minute seizure. The dispatcher states collateral from friends indicates they have attended a ‘rave dance concert’
- State 5 modifications to the standard status epilepticus algorithm in the setting of suspected toxin induced seizures
Vital signs on arrival to ED:
-HR: 144 -Temp: 38 -BP: 195/110 -GCS: 8 (E2V2M4) -RR: 22
She is no longer seizing, she is drenched in sweat, her skin is flushed and red, she has dilated pupils, increased muscular tone and hyperreflexia
Initial lab results:
-pH: 7.20, pCO2: 88, HCO3: 8, Na: 120, K: 4, Cl: 100
-Urea: 3, Cr: 88, glucose: 2.8, ALT: 422, AST: 333
-ALP: 222, albumin: 33, bilirubin: 4, GGT: 115
a. Provide interpretation (5)
b. List 5 differential diagnoses with rationale and testing needed to confirm
c. State 6 goals of management and how you will achieve them
Consider antidote: sodium bicarbonate, pyridoxine
1st line benzodiazepines
2nd line Phenobarbitone, Propofol
Avoid phenytoin (sodium channel blockers)
Naloxone used for hypoxic seizures secondary to opioids
a.
Normal anion gap metabolic acidosis (AG 12), uncompensated, respiratory acidosis secondary possible hypoventilation +/- V/Q mismatch
Critical hyponatraemia with reduced serum osmolality (246mosm/kg) - water ingestion and possible SiADH secondary to MDMA
Liver impairment - secondary to MDMA, ischaemia, paracetamol toxicity
Hypoglycaemia - exertional
Sympathomimetic toxidrome –> seizure
b.
Meningitis/ encephalitis
-Blood cultures, delayed lumbar puncture, WBC, CRP
MDMA toxicity leading to sympathomimetic toxidrome and hyponatraemia secondary to SiADH
Thyroid storm
SAH - CT, CTA, delayed LP
Serotonin syndrome
-Fever, increased tone, clonus
c.
Airway management
-Intubate and ventilate
-RSI: Fentanyl 4mcg/kg, rocuronium, 1.5mg/kg, ETT 6.5, LMA 4, SIMV TV 6ml/kg
Manage hypertension
-First line benzodiazepine e.g. midazolam 5mg IV prn
-Second line GTN infusion 10mcg/ml, labetalol 10-20mg q10 mins, infusion 2mg/min
Correct hypoglycaemia
-50ml of 50% dextrose
Correct hyponatraemia
-3ml of 3% hypertonic saline
Manage/ prevent further seizure
-Continuous EEG monitoring
-Midazolam infusion
Cover for sepsis
-Antibiotics/ antivirals
Mange hyperthermia
-Ice packs to axilla, groin
-If temperature > 39.5 then active cooling with paralysis, cooled fluids, cooling blanket, bladder lavage, ECMO
Disposition / facilitate further investigation
-ICU, liaise with toxicology team, CT brain and chest, antidote cyproheptadine 12mg PO/IV for serotonin syndrome
A 55 year old farmer has been brought to your ED after a sudden collapse in his paddock
You suspect he may have been bitten by a snake
Ambulance offices state he has 2 puncture marks to his left ankle. A pressure immobilisation bandage has been applied. The patient is alert
- List 5 key differential diagnosis other than snake bite you would consider in this presentation and how you would initially assess for each
- List 4 examination findings you would seek on initial assessment that would support a diagnosis of envenomation
- List 3 investigations with justification which may help in assessment / treatment of this patient
- List 3 criteria that need to be satisfied for you to remove the patients PIB
- List 3 factors you will consider when determining the type of monovalent antivenom to administer this patient if evenomation is confirmed
1.
Cardiac
-Dysrhythmia, ACS, aortic dissection
-Clinical history, ECG, troponin
Respiratory
-Pulmonary embolism
-Clinical history, raised JVP, DVT, ECG, D-dimer
Environment
-Exertional heat stroke
-Temperature, CK level, renal function, AMS
Sepsis
-Meningoencephalitis
-Septic screen
CNS - SAH
-Pupils, GCS, weakness
Toxins
-CCB, digoxin, organophosphate poisoning
-Psych history, ECG
-Bite mark
-Descending flaccid paralysis
-Bleeding, pain
-Nausea, vomiting, tachycardia
-Myotoxicity - haematuria, rhabdomyolysis
Coagulation studies / d-dimer
-INR > 3 VICC
CK
FBC
-Anaemia, thrombocytopenia, MAHA
-Abnormal exam or labs = antivenom 1 vial for adults and children
-Normal exam and labs = PBI removed, if deterioration then reapplied and labs repeated, antivenom administered
-If no deterioration post PBI removal do exam and bloods at 1 hour, 6 hours and 12 hours
-Discharge if no evidence of envenoming at 12 hours post bite
-Type of snake
-Geography
-Syndrome/ toxicology advice/ SVDK
A 60 year old presents to ED 2 hours after a confirmed intentional ingestion of 20 tablets of diltiazem 240mg
Currently asymptomatic
GCS: 15
HR: 60
BP: 120/80
RR: 18
Sats: 96% on RA
Temp: 36.5
- Outline your initial risk assessment and further information you require
- List options for decontamination with justification
The patients condition deteriorates
-GCS: 15
-BP: 80/40
-HR: 40
- Outline your management
-Life threatening toxic ingestion expecting refractory hypotension, multiorgan failure and shock, requires immediate aggressive management in resus with calcium, inotropes, fluids
-Time
-Formulation - slow release, immediate release
-Coingestants - Beta blocker, alcohol
-Patient weight
-Vomiting
-Comorbidities - heart failure, renal failure
Activated charcoal 50g PO/BG
-Minimise absorption
-Consider intubation to facilitate
Whole bowel irrigation
-Decrease absorption, particularly if sustained release
Activated charcoal/ WBI within 1-2 hours, if sustained release up to 4 hours
IVF - sodium chloride 0.9% aiming MAP > 50
Atropine 600mcg IV up to 3 doses
High dose euglycaemic therapy
-50ml of 50% dextrose
-1unit/kg of insulin bolus
-Followed by 50ml of 50% dextrose and 1 unit/kg of insulin over 1 hour
Escalate to noradrenaline/ adrenaline infusion 0.05mcg/kg/min
Calcium 10-20ml of 10% calcium gluconate, can repeat up to 3 doses
External pacing
Intravenous lipid emulsion 1.5ml/kg of 20%
Disposition
-ICU, toxicology
-ECMO
A 28 year old male is brought to ED by ambulance after concerns from his family regarding agitation and altered mental status. During triage he becomes increasingly verbally and physically aggressive and he tries to get off the ambulance trolley
GCS: 14
HR: 125
BP: 140/90
RR: 26
Sats: 99% on RA
Temp: 37.9
- List 5 tox and 5 non tox causes for this presentation
- List 4 escalating steps to manage this behaviour
- List 4 medications that could be used to manage the behaviour include doses
Encephalitis
Traumatic head injury - Subdural haemorrhage
Thyroid storm
Primary psychosis - schizophrenia
Metabolic - hyponatraemia
Sympathomimetic toxidrome - amphetamine
Anticholinergic syndrome - TCA
Alcohol ingestion - ethanol, methanol
Serotonergic syndrome - SSRI
Sedative hypnotic withdrawal - e.g. benzodiazepine withdrawal
-Show of force - code black, verbal deescalation
-Oral sedation - diazepam, olanzapine
-Physical restraint/ duty of care
-Parental IM/IV
PO diazepam 10mg
PO olanzapine 10mg
IM/ IV midazolam 10mg
IV/ IM droperidol 10mg
Ketamine 4mg IM
A 20 year old mechanic apprentice is brought to your ED after an intentional overdose of 200ml of antifreeze containing ethylene glycol 30 minutes ago
GCS: 15
HR: 90
BP: 110/80
RR: 20
Sats: 99% on RA
Temp: 36.5
- Outline your risk assessment based on the information provided
- List 4 investigations, their anticipated abnormality in this patient, the rationale for their use in this patient
- List 2 temporising measures for managing this severe toxicity
- Outline the definitive treatment of severe toxicity with indications and endpoints
-This is a life threatening toxic ingestion of ethylene glycol (>1ml/kg) expecting reduced level of consciousness, metabolic acidosis, hypoglycaemia, hypoglycaemia. Will require haemodialysis.
ABG
-Determine anion gap
-Raised anion gap acidosis
-Surrogate marker for toxicity
Serum osmolality and sodium, glucose, urea
-Enable calculation of osmolar gap
-A gap > 10 consistent with toxic alcohol ingestion
Calcium level
-Ethylene glycol causes calcium oxalate crystals which precipitate in tissues
-This results in hypocalcaemia
-Surrogate marker of toxicity
Ethanol level
-If raised
-Would lead to delayed onset toxicity
Urine microscopy
-Calcium oxalate crystals
-Pathognomonic
-Ethanol PO/NG, initially 3 40ml shots, then 1 shot per hour
-Fomepizole 15mg/kg IV
-Sodium bicarbonate - 1-2mmol/kg aiming pH > 7.3
-RSI with hyperventilation
-Calcium gluconate 10-20ml of 10%
-50ml of 50% dextrose if hypoglycaemia
-Pyridoxine/ thiamine
Haemodialysis
Indications
-Acidosis pH < 7.3 (refractory), AKI, OG > 20
-End points would be normalisation of serum levels
-Normalisation of osmolar gap
-Normalisation of anion gap
