Acute medicine Flashcards
ABCDE protocol
Airway
- assess: patency, secretions/vomit, obstruction
- manage: airway manoeuvres, suction, airway adjunct
Breathing
- assess: RR, O2 sats, palpation/percussion/auscultations, later CXR
- manage: O2
Circulation
- asses: HR + BP, cap refill/perfusion, cyanosis, auscultation
- manage: fluids, bloods/ABG
Disability
- asses: AVPU/GCS, glucose, PEARL
Exposure
- assess: whole body inspection
*Use SBAR for handover: situation, background, assessment, recommendation
Why does alcohol withdrawal occur?
Alcohol is a depressant (GABA agonist) so chronic use leads to upregulation of glutamate receptors
When alcohol is removed, the upregulation of glutamate receptors means there is an increase in CNS stimulation thus there is a gradula increase in CNS overactivity
Timeline of alcohol withdrawal
Minor 6hrs
- anxiety, tremor, palpitations, GI upset
Hallucinations 12hrs
Seizures 32 hrs
- short, generalised tonic-clonic seizures
Delirium tremens 48hrs
- delirium, severe tremor, fever, FATAL
Ddx of delirium tremens
Acute liver failure
- ammonia (encephalopathy), albumin (ascites + peripheral oedema), bilirubin (jaundice), blood factors (bruising)
Wernicke’s encephalopathy
- Confusion, Ataxia, Nystagmus
Hx and O/E of alcohol withdrawal
CAGE question./longer AUDTI question.
Signs of alcohol abuse (smell, hygiene etc.)
Chronic liver disease signs
Mx of alcohol withdrawal
1) Benzodiazepines (chlordianzepoxide, diazepam)
2) Pabrinex (B1 to prevent Wernicke’s)
3) Glucose (if hypo + needed with pabrinex)
4) Manage alcohol dependence (Drug+Alcohol Liaison specialist, therapy)
What scale is used to assess severity of alcohol withdrawal?
CIWA-Ar scale
- Nausea/vomiting
- Tremor
- Paroxysmal sweats
- Anxiety
- Agitation
- Tactile disturbances
- Auditory disturbances
- Visual disturbances
- Headache/fullness in head
- Orientation/clouding of sensorium
- dw don’t need to memorise
What should you also consider if you suspect alcohol withdrawal?
Hypoglycaemia
Electrolyte distubrances
Hepatic encephalopathy
Anaphylaxis presentation
Airway = throat/tongue swelling, stridor
Breathing = SOB, increased HR, decreased O2
Circulation = SHOCK; decreased BP, increased HR, low consciousness
Shin/mucosal = uritcaria + angioedema, flushing
Sense of impeding doom
What causes anaphlyaxis?
Life-threatening, systemic, hypersensitivity reaction
- mast-cell/basophil degranulation
- increased capillary permeability, bronchospasm, decreased vascular tone
3 common triggers
1) Food (child) - nuts
2) Drugs/chemicals (adults) - penicillin
3) Toxins - bee/wasp stings
* RF = Hx of atopy
Mx of anaphylaxis
I. HELP II. Remove trigger III. Lie flat and raise legs IV. IM adrenaline 0.5mg 1:1000 V. Airway, breathing, circulation VI. IV chlorpheniramine + IV hydrocortisone
What further ix could confirm anaphylaxis?
Increased serum tryptase and plasma histamine on blood tests
What should follow up involve after an anaphylaxis reaction?
Refer to immunology/allergy clinic
- RAST specific IgE testing to determine allergies
Provide EpiPen and education re anaphylaxis
Get a medic alert bracelet
Poisoning summary card
Administration of XS pharmaceutical agent
- accidental in <10yo, deliberate >10yo (typically alcohol in 15-35 yo)
Ix
- ABCDE, ABG, ECG, FBC, U&E, LFT, INR, glucose, paracetamol + salicylate levels
Mx
- TOXBASE, National Poisons Information Service
- consider activated charcoal if = 4hrs to reduce absorption of drug
- consider gastric lavage (rare)
Compare early and late presentations of aspirin overdose
Early
- N&V, diarrhoea
- ‘per-spirin-g’ = hyperthermia, sweating
- ‘raspi-irin’ = hyperpnoea (stimulates respiratory centre in medula)
- ‘aspirin-ging’ = tinnitus, deafness, dizziness
Late/severe
- pulmonary oedema
- decreased BP and heart block
- seizures + decreased GCS
What counts as an aspirin overdose and what would lab results show?
> 150mg/kg, severe if >500mg/kg
Lab results:
Early => early respiratory alkalosis
Late => high anion gap metabolic acidosis
Mx of aspirin OD
Urine alkalinsation with IV sodium bicarbonate
Dialysis
Timeline of paracetamol sx
Often asymptomatic presentation
Timeline:
<24hr = mild N&V, lethargy
24-72hr = RUQ pain, vomiting, hepatosplenomegaly
>72 hr = acute liver failure
How does a paracetamol OD lead to liver failure?
XS paracetamol is metabolised by CYP450 in the liver to NAPQ1, which is then conjugated to glutathione and excreted
XS means glutathione is depleted and toxic NAPQ1 accumulates, causing hepatocyte necrosis :(
What dose is a paracetamol OD and how is it managed?
> 150mg/kg, 12g can be fatal
Mx:
- IV N-acetyl-lysteine if below treatment line (graph used to determine)
- liver transplant
What does opiate OD result in and how is it treated?
CNS depression
- respiratory depression
- bradycardia, hypotension
- pinpoint pupils
- late/severe: low GCS/coma
IV naloxone (muscarinic receptor antagonist)
When is a catheter indicated?
Urinary retention and to monitor urine output
Types of blood transfusions
X-match for: Packed red cells - indicated if Hb <7g/l or 30% loss of blood volume - 1 unit increases Hb by 10-15g/l Platelets - when plts <20x10[unit] FFP - correct clotting factors => DIC
Complications of blood transfusions
EARLY (<24hrs) Febrile non-haemolytic reaction Anaphylaxis Acute haemolytic reaction Bacterial infection Transfusion associated circulatory overload or transfusion associated lung injury
LATE (>24hrs) Iron overload Transfusion associated graft vs host disease Infection Delayed haemolytic reaction