Hi orris
Hi Dr Afzal Khan ( Pharm. D) here
Just here for ward round practice
Like I am here for a teaching round, through a case and teach me
Can I have a look of patient egfr and BNP
| Test | Result | Reference Range | Flag |
|---|---|---|---|
| eGFR | 38 mL/min/1.73mΒ² | >60 | π΄ LOW |
| BNP | 1,840 pg/mL | <100 pg/mL | π΄ HIGH |
| Creatinine | 187 Β΅mol/L | 60-110 | π΄ HIGH |
| Urea | 11.2 mmol/L | 2.5-7.8 | π΄ HIGH |
| NaβΊ | 134 mmol/L | 135-145 | π‘ LOW |
| KβΊ | 5.1 mmol/L | 3.5-5.0 | π‘ BORDERLINE HIGH |
| Glucose | 14.2 mmol/L | 4.0-7.8 | π΄ HIGH |
| HbA1c | 9.1% | <6.5% | π΄ HIGH |
| ECG | Atrial Fibrillation - no acute ST changes | - | π΄ |
ΒΉ BNP indicates Acute decompensated Heart Failure 2- Metformin dose should be adjusted, Ramipril should be avoided 3- AFib leads to introduction of Warfarin
| Drug | Consideration in this patient |
|---|---|
| Apixaban | β Preferred - safest in CKD, least renal clearance (~27%) |
| Rivaroxaban | π‘ Use with caution in CKD |
| Dabigatran | π΄ Avoid - 80% renal clearance, eGFR 38 is risky |
| Warfarin | π‘ Still used in valvular AF or eGFR <15, but NOT first choice here |
| Drug | Action | Reason |
|---|---|---|
| Metformin | Hold/reduce | AKI + acute illness |
| Ramipril | Hold temporarily | AKI, hyperkalaemia risk |
| Amlodipine | Review - can worsen peripheral oedema | |
| Add IV Furosemide | For acute decongestion | ADHF |
| Add Apixaban | AF anticoagulation | After CHAβDSβ-VASc scoring |
Calculate CHA2DS2-VASc score for AFib stroke risk
| Letter | Risk Factor | Points | Mr. Tariq | Score |
|---|---|---|---|---|
| C | Congestive Heart Failure | 1 | β Yes (ADHF confirmed) | 1 |
| H | Hypertension | 1 | β Yes (known + BP 158/94) | 1 |
| Aβ | Age β₯ 75 years | 2 | β He is 64 | 0 |
| D | Diabetes Mellitus | 1 | β Yes (T2DM) | 1 |
| Sβ | Prior Stroke/TIA | 2 | β Not mentioned | 0 |
| V | Vascular Disease (MI, PVD) | 1 | β Yes (previous MI) | 1 |
| A | Age 65-74 years | 1 | β He is 64... almost! | 0 |
| Sc | Sex Category (Female) | 1 | β Male | 0 |
| Score | Annual Stroke Risk | Recommendation |
|---|---|---|
| 0 (male) | ~0% | No anticoagulation needed |
| 1 (male) | ~1.3% | Consider anticoagulation |
| 2+ | β₯2.2% | Anticoagulation recommended |
| 4 | ~4% | Anticoagulation strongly indicated |
| Apixaban | Rivaroxaban | Dabigatran | Warfarin | |
|---|---|---|---|---|
| Renal clearance | ~27% | ~33% | ~80% | Minimal |
| eGFR 38 safe? | β Yes | π‘ Caution | π΄ Avoid | π‘ Option |
| Dosing in this patient | 5mg BD (check dose reduction criteria) | - | - | - |
Always calculate CHAβDSβ-VASc before choosing the anticoagulant, and always check renal function before dosing the DOAC. These two steps together prevent both under-treatment (stroke) and over-treatment (bleeding).
Let's start this day with new case
You explain this to me
| Finding | Why It Worries You |
|---|---|
| BP 182/110 | Hypertensive emergency? Hypertensive encephalopathy? |
| GCS 13 | Reduced consciousness - not just a post-ictal state |
| Severe headache + vomiting | Classic signs of raised intracranial pressure |
| Seizure in known epileptic | Could be breakthrough seizure OR provoked seizure |
| On Phenytoin | Is her drug level therapeutic? |
| Test | Why |
|---|---|
| Blood glucose (BM) | Hypoglycaemia causes seizures + confusion |
| ECG | Rule out cardiac arrhythmia |
| 12-lead ECG | Phenytoin can cause cardiac conduction issues |
| Test | Why |
|---|---|
| Phenytoin level | Is she toxic or subtherapeutic? |
| FBC | Infection, anaemia |
| U&E + Creatinine | Renal function - affects drug dosing |
| LFTs | Phenytoin is hepatically metabolised |
| Calcium, Magnesium | Low levels trigger seizures |
| TFTs | She's on Levothyroxine - is she over/under replaced? |
| CRP/ESR | Infection/inflammation |
| Test | Why |
|---|---|
| CT Head (urgent, non-contrast) | Rule out bleed, mass, raised ICP |
| LP (after CT) | If CT clear and SAH suspected - xanthochromia |
Mrs. Nadia = Confused + Seizure + Severe Headache + BP 182/110
β
Rule out: SAH / ICH / Hypertensive encephalopathy
β
Check: Phenytoin level + CT Head URGENTLY
β
Pharmacist priorities: Phenytoin level, drug interactions,
BP management strategy, Levothyroxine adequacy
I think the combination of anti htn and levothyroxine is causing Htn crisis
| Scenario | Effect on BP |
|---|---|
| Levothyroxine overdose / hyperthyroidism | Can raise BP, increase HR, cause palpitations |
| Levothyroxine at therapeutic dose | Generally does NOT cause hypertensive crisis |
| Hypothyroidism (undertreated) | Can actually CAUSE or WORSEN hypertension |
| Interaction | Mechanism | Effect |
|---|---|---|
| Phenytoin + Amlodipine | Phenytoin induces CYP3A4 | Amlodipine levels reduced - less BP control |
| Phenytoin + Lisinopril | No major PK interaction | Minimal |
| Cause | Clues in This Case |
|---|---|
| Hypertensive encephalopathy | BP 182/110 + confusion + headache + seizure |
| Subarachnoid haemorrhage | Sudden severe headache + vomiting + seizure |
| Reduced antihypertensive efficacy | Phenytoin-Amlodipine interaction |
| Non-compliance | Common, always ask |
| Secondary hypertension | Renal, endocrine - less likely acutely |
As a clinical pharmacist, your role is to identify drug interactions that reduce therapeutic efficacy - in this case, Phenytoin reducing Amlodipine levels is a real and clinically relevant interaction that may be contributing to poor BP control.
"Hyperdense area noted in the basal cisterns. Appearances consistent with subarachnoid haemorrhage. No midline shift."
I think now bp reduction is nessary upto 160 mm hg,to reduce sah complication ,
| Guideline | Target |
|---|---|
| AHA/ASA SAH Guidelines | Systolic <160 mmHg until aneurysm secured |
| Neurocritical Care Society | SBP <160 mmHg, avoid MAP <70 mmHg |
| Key principle | Reduce BP - but not too fast, not too low |
| Drug | Use in SAH | Reason |
|---|---|---|
| IV Labetalol | β First choice | Titratable, alpha+beta blockade, proven in neurocritical care |
| IV Nicardipine | β Good option | CCB, smooth BP control, neuroprotective properties |
| IV Hydralazine | π‘ Use with caution | Unpredictable, reflex tachycardia |
| IV GTN/Nitroprusside | π΄ Avoid | Causes cerebral vasodilation β raises ICP |
| Oral Amlodipine | π΄ Not suitable acutely | Too slow, cannot titrate |
| Oral Lisinopril | π΄ Not suitable acutely | Not titratable in emergency |
| Detail | |
|---|---|
| Drug | Nimodipine (oral/NG) |
| Dose | 60mg every 4 hours for 21 days |
| Mechanism | CCB - prevents cerebral vasospasm |
| Purpose | Reduces delayed ischaemic neurological deficit (DIND) |
| Start timing | As soon as SAH confirmed |
| Effect on BP | Can lower BP - monitor carefully |
| Route | Oral or NG (IV formulation causes severe hypotension - different concentration!) |
β οΈ Critical safety point: IV Nimodipine and oral Nimodipine are NOT interchangeable in terms of route/concentration. IV given orally or oral given IV has caused fatal errors. This is a well-documented medication error in SAH management.
| Drug | Action | Reason |
|---|---|---|
| Amlodipine 10mg oral | Hold | Not suitable for acute BP control |
| Lisinopril 10mg oral | Hold | Not suitable for acute BP control |
| Start IV Labetalol | Titrate to SBP 140-160 | Acute BP control |
| Start Nimodipine 60mg PO/NG Q4H | Start immediately | Prevent vasospasm - 21 day course |
| Phenytoin | Review level urgently | Seizure management - see below |
| Question | Answer |
|---|---|
| Continue Phenytoin? | Check level first |
| If subtherapeutic | IV loading dose needed |
| If toxic | Hold and monitor |
| Alternative? | Levetiracetam increasingly preferred in SAH (less drug interactions, no CYP induction) |
| Prophylactic anticonvulsants in SAH? | Controversial - guidelines suggest short-term only (not long-term routine prophylaxis) |
SAH Confirmed β
1. Neurosurgical referral (urgent - aneurysm clipping/coiling)
2. IV Labetalol β titrate SBP to 140-160 mmHg
3. Nimodipine 60mg Q4H PO Γ 21 days (vasospasm prevention)
4. Check Phenytoin level β manage accordingly
5. Strict bed rest, analgesia (paracetamol Β± codeine)
6. Avoid NSAIDs (bleeding risk)
7. DVT prophylaxis - mechanical only initially (TED stockings)
8. Stool softeners (avoid Valsalva - raises ICP)
Nsaid should be avoided here , does team wants to intubated patient
| Reason | Mechanism |
|---|---|
| Antiplatelet effect | COX-1 inhibition β reduced thromboxane A2 β impaired platelet aggregation β increased bleeding risk |
| Rebleeding risk | Already fragile aneurysm + antiplatelet effect = catastrophic |
| Renal effects | Reduce renal perfusion - already a concern in critically ill |
| Drug | Recommendation | Notes |
|---|---|---|
| Paracetamol 1g QDS | β First line | Safe, no bleeding risk |
| Codeine 30-60mg QDS | β Second line (with caution) | Mild opioid, watch for constipation - important! Straining raises ICP |
| IV Morphine | π‘ For severe pain, short-term | Monitor sedation, respiratory depression |
| Aspirin | π΄ Avoid | Antiplatelet |
| NSAIDs | π΄ Avoid | As above |
| Tramadol | π΄ Caution/Avoid | Lowers seizure threshold - dangerous in this patient |
β οΈ Pharmacist pearl: Always prescribe a laxative alongside opioids in SAH. Constipation β straining β Valsalva β raised ICP β rebleeding. This is a simple but life-saving prescription.
| GCS | Airway Decision |
|---|---|
| GCS β₯ 13 | Monitor closely, may not need intubation yet |
| GCS 9-12 | Strong consideration for intubation |
| GCS β€ 8 | Intubate - airway not protected |
| Indication | Present in Mrs. Nadia? |
|---|---|
| GCS β€ 8 | β Not yet (GCS 13) |
| Falling GCS | β Monitor |
| Airway not protected | β Not yet |
| Refractory seizures | β Single seizure so far |
| Respiratory failure (SpOβ <92%) | β Currently 96% |
| Going to CT/angiography and combative | π‘ Possible |
| Pre-operative (before coiling/clipping) | β Will need it then |
| Drug | Role | SAH Consideration |
|---|---|---|
| Propofol | Induction | β Good - also reduces ICP |
| Ketamine | Induction | π΄ Traditionally avoided - raises ICP (though evidence evolving) |
| Thiopentone | Induction | β Reduces ICP - used in neurocritical care |
| Suxamethonium | Paralytic (RSI) | π‘ Caution - brief ICP rise with fasciculations |
| Rocuronium | Paralytic (RSI) | β Preferred - no ICP concerns |
| Fentanyl pre-treatment | Blunt intubation response | β Reduces BP/ICP spike during laryngoscopy |
| Parameter | Target | Why |
|---|---|---|
| PaCOβ | 35-40 mmHg | Avoid hypercapnia (raises ICP) AND hypocapnia (causes vasoconstriction) |
| PaOβ | >80 mmHg | Avoid hypoxia |
| SBP | 140-160 mmHg | Maintain as before |
| Sedation | Light as possible | Allow neuro assessment |
Right now:
- No mandatory intubation indication (GCS 13)
- Monitor GCS every 15-30 minutes
- If GCS drops to β€8 or airway concern β intubate with RSI
- Neurosurgical team to decide timing for angiography/coiling
- Pre-procedure intubation likely needed
Pharmacist actions:
β
Nimodipine 60mg Q4H started
β
IV Labetalol titrating to SBP 140-160
β
Paracetamol 1g QDS for analgesia
β
Laxative prescribed (lactulose/senna)
β
Phenytoin level checked
β
NSAIDs avoided
β
RSI drugs prepared and checked if intubation needed
I am unaware of this can you pls explain
Normal aneurysm treatment options:
1. Surgical clipping - open brain surgery, metal clip placed on aneurysm neck
2. Endovascular coiling - minimally invasive, done via groin artery
Groin artery (femoral)
β
Catheter threaded up to brain vessels
β
Platinum coils pushed into aneurysm sac
β
Coils cause clot formation INSIDE aneurysm
β
Aneurysm excluded from circulation β no more bleeding risk
| Problem | Consequence |
|---|---|
| Coils are a foreign body in blood vessel | Can trigger clot formation on coils β stroke |
| Patient just had a brain bleed (SAH) | Anticoagulation/antiplatelets β rebleeding risk |
| Drug | Use | Detail |
|---|---|---|
| IV Heparin | β Given during procedure | Prevents thrombus forming on catheter/coils during coiling |
| Dose | Weight-based bolus | Usually 70-100 units/kg |
| Monitoring | ACT (Activated Clotting Time) | Target ACT 250-300 seconds during procedure |
| After procedure | Heparin stopped | Reversed or allowed to wear off |
| Drug | Recommendation |
|---|---|
| Antiplatelets | Usually NOT required post-procedure |
| Reason | No stent = no risk of in-stent thrombosis |
| Anticoagulation | Not routinely continued |
| Drug | Recommendation |
|---|---|
| Aspirin 75mg + Clopidogrel 75mg | β Dual antiplatelet therapy (DAPT) required |
| Duration | Typically 3-6 months then aspirin alone |
| Reason | Stent in brain vessel β high thrombosis risk without DAPT |
| Start timing | Ideally pre-loaded before procedure if planned |
She just had SAH (brain bleed)
+
May need stent-assisted coiling
+
Already on Nimodipine (which lowers BP)
β
DAPT (Aspirin + Clopidogrel) needed for stent
β
But DAPT increases rebleeding risk in early SAH!
| Timing | Strategy |
|---|---|
| Pre-procedure | Neurosurgeon + interventional neuroradiologist decide stent vs no stent |
| If simple coiling | No DAPT needed - safer for SAH patient |
| If stent essential | DAPT started, risk of bleeding accepted as lesser evil vs stroke |
| First 24-48 hours post-SAH | Avoid antiplatelets if possible |
| Interaction | Detail |
|---|---|
| Nimodipine + Antiplatelets | No direct pharmacokinetic interaction |
| Nimodipine + BP lowering | Nimodipine itself lowers BP - adding antihypertensives needs careful monitoring |
| Key concern | Nimodipine + IV Labetalol β additive BP lowering β watch for hypotension |
| Nimodipine + CYP3A4 drugs | Nimodipine is CYP3A4 substrate - check for interactions |
After endovascular coiling in SAH:
1. Was a stent used?
β YES: Start DAPT (Aspirin + Clopidogrel) - liaise with neurosurgeon for timing
β NO: No routine antiplatelet needed
2. Continue Nimodipine 60mg Q4H Γ 21 days (vasospasm prevention - non-negotiable)
3. Monitor BP: SBP 140-160 mmHg (pre-aneurysm securing)
After securing: some centres allow slightly higher BP to prevent vasospasm
4. DVT prophylaxis:
β Mechanical (TED stockings, pneumatic compression) first
β LMWH only after aneurysm secured + neurosurgical approval
5. Watch for post-procedure complications:
β Vasospasm (Days 4-14 post SAH) - most dangerous period
β Hydrocephalus
β Hyponatraemia (SIADH or cerebral salt wasting - common in SAH)
| Concept | Remember |
|---|---|
| Coiling = foreign body | Needs heparin during procedure |
| Stent used = DAPT needed | Aspirin + Clopidogrel post-procedure |
| No stent = no routine DAPT | Safer in SAH |
| Nimodipine continues regardless | 21 days, every 4 hours, vasospasm prevention |
| Nimodipine route safety | NEVER give oral Nimodipine IV - fatal error |
| Post-SAH hyponatraemia | Common complication - monitor Na daily |
Yeah weap up
| Original Medication | Action Taken | Reason |
|---|---|---|
| Phenytoin 300mg ON | Check level β adjust | Seizure management, narrow TI drug |
| Levothyroxine 100mcg OD | Continue | Hypothyroidism - do not stop |
| Amlodipine 10mg OD | Held acutely | Not titratable in emergency |
| Lisinopril 10mg OD | Held acutely | Not titratable in emergency |
| New Medication Added | Dose | Indication |
|---|---|---|
| IV Labetalol | Titrate to SBP 140-160 | Acute BP control |
| Nimodipine | 60mg PO/NG Q4H Γ 21 days | Cerebral vasospasm prevention |
| Paracetamol | 1g QDS | Analgesia - safe in SAH |
| Lactulose/Senna | OD/BD | Prevent straining β raised ICP |
| Heparin | Intra-procedure only | Prevent coil thrombosis during coiling |
| TED stockings | Apply immediately | DVT prophylaxis (mechanical only initially) |
| Drugs Avoided | Reason |
|---|---|
| NSAIDs | Antiplatelet effect β rebleeding |
| Aspirin | Antiplatelet β rebleeding |
| Tramadol | Lowers seizure threshold |
| GTN/Nitroprusside | Cerebral vasodilation β raises ICP |
| Ketamine | Raises ICP |
| Area | Performance |
|---|---|
| Identifying NSAIDs danger | β Excellent |
| BP reduction target | β Correct |
| Thinking about intubation | β Great proactive thinking |
| Levothyroxine-HTN link | π‘ Good thinking, needed refinement |
| Anticoagulation post-coiling | π New learning - well received |
Let's go with new case
As I am a clinical pharmacist, diagnosis is not my part but still I can tell, this bleed is due to varices which is common in chr alc liver disease
Chronic alcohol use
β
Liver cirrhosis (Child-Pugh B confirmed)
β
Portal hypertension (increased pressure in portal vein)
β
Blood diverts to collateral vessels
β
Oesophageal varices form (thin-walled, high pressure)
β
Rupture β massive haematemesis
Ibuprofen 400mg TDS - self-prescribed!
| Problem | Detail |
|---|---|
| NSAIDs in cirrhosis | Cause gastric mucosal damage β peptic ulcer β bleed |
| NSAIDs + portal hypertension | Dramatically worsen GI bleeding risk |
| NSAIDs + liver disease | Reduced prostaglandin synthesis β renal vasoconstriction β hepatorenal syndrome risk |
| NSAIDs + Spironolactone | Blunt diuretic effect, worsen fluid retention |
| Finding | Significance |
|---|---|
| BP 88/54 mmHg | Hypotensive - haemorrhagic shock |
| HR 118 bpm | Compensatory tachycardia |
| Pallor + cold peripheries | Poor peripheral perfusion |
| SpOβ 95% | Borderline |
1.0 = significant haemorrhage
1.4 = massive haemorrhage, life threatening
| Product | Action | Detail |
|---|---|---|
| IV access | 2 large bore cannulas | Immediate |
| IV Crystalloid | Cautious fluid resuscitation | Target SBP >90 - avoid over-resuscitation in cirrhosis (worsens portal pressure) |
| Blood transfusion | Urgent crossmatch | Transfuse if Hb <70 g/L (restrictive strategy in varices - overtransfusion raises portal pressure) |
| FFP + Platelets | If coagulopathic | Cirrhosis = impaired clotting factor synthesis |
| Drug | Dose | Mechanism | Duration |
|---|---|---|---|
| Terlipressin | 2mg IV Q4H (then 1mg Q4H after haemostasis) | Splanchnic vasoconstriction β reduces portal pressure β slows variceal bleeding | 5 days |
| Alternative: Octreotide | 50mcg bolus then 50mcg/hr infusion | Somatostatin analogue β reduces splanchnic blood flow | 5 days |
β οΈ Start Terlipressin BEFORE endoscopy - do not wait. Every minute of active variceal bleeding increases mortality.
| Drug | Dose | Why? |
|---|---|---|
| IV Ceftriaxone 1g OD | 5-7 days | Cirrhotic patients have high infection risk post-bleed. Bacterial infection worsens portal hypertension and increases rebleeding. Antibiotics reduce mortality in variceal bleeding - NICE/BSG guideline recommendation |
| Alternative (if penicillin allergy) | Ciprofloxacin 400mg IV BD |
| Consideration | Detail |
|---|---|
| GCS 15 currently | Not indicated now |
| Active haematemesis | Risk of aspiration |
| Pre-endoscopy | Anaesthetist should assess |
| If GCS drops or massive rebleed | Intubate before endoscopy |
| Drug | Action | Reason |
|---|---|---|
| Ibuprofen | STOP immediately | GI bleed risk, renal risk in cirrhosis, worsens bleeding |
| Metformin | Hold | Haemodynamic instability + shock = lactic acidosis risk |
| Propranolol | Hold acutely | Beta-blocker masks tachycardia (your only sign of bleeding severity), can worsen hypotension in shock |
| Spironolactone | Hold | AKI risk in haemodynamic shock |
Mr. Imran - Variceal Bleed + Haemorrhagic Shock
IMMEDIATE:
β
2x large bore IV access
β
Cautious IV fluids (crystalloid)
β
Crossmatch 4 units blood
β
Terlipressin 2mg IV NOW
β
Ceftriaxone 1g IV NOW
β
Stop Ibuprofen, Metformin, Propranolol, Spironolactone
β
Urgent endoscopy (within 12 hours per BSG guidelines)
β
Involve GI team + ITU
MONITORING:
- BP, HR every 15 minutes
- Urine output (catheterise)
- Hb, coagulation, U&E, LFTs, ammonia
Can you tell
Liver cirrhosis β liver cannot detoxify ammonia
β
Ammonia (NH3) accumulates in blood
β
Crosses blood-brain barrier
β
Astrocyte swelling + neurotransmitter disruption
β
Brain dysfunction β confusion, agitation, coma
| Trigger | Mechanism |
|---|---|
| GI bleed itself | Blood in gut = protein load = ammonia production by gut bacteria |
| Dehydration/shock | Reduced renal ammonia clearance |
| Infection | Ceftriaxone treating this, but early infection already stresses liver |
| Constipation | Increased ammonia absorption from gut |
The GI bleed is the classic precipitant of HE - blood is protein, gut bacteria digest it, produce massive ammonia load.
| Grade | Symptoms | Mr. Imran? |
|---|---|---|
| Grade 0 | No symptoms | |
| Grade 1 | Mild confusion, sleep disturbance | |
| Grade 2 | Disorientation, inappropriate behaviour | β Likely here |
| Grade 3 | Somnolent but rousable, gross disorientation | |
| Grade 4 | Coma, no response |
| Detail | |
|---|---|
| Drug | Lactulose |
| Dose | 30-50ml every 1-2 hours until bowels open, then titrate to 2-3 soft stools/day |
| Mechanism | Acidifies gut β converts NH3 (absorbable) to NH4βΊ (non-absorbable) β trapped in gut β excreted in stool |
| Also | Acts as osmotic laxative β flushes ammonia-producing bacteria out |
| Target | 2-3 soft stools per day - this is how you know it's working |
| Route | Oral or NG tube if cannot swallow |
Lactulose mechanism:
Gut pH lowered by lactulose
β
NH3 + HβΊ β NH4βΊ
β
NH4βΊ cannot cross gut wall
β
Excreted in faeces
β
Blood ammonia falls
β
Brain function improves
| Detail | |
|---|---|
| Drug | Rifaximin |
| Dose | 550mg BD |
| Mechanism | Non-absorbable antibiotic β kills ammonia-producing bacteria in gut |
| Use | Added to Lactulose for recurrent or refractory HE |
| Advantage | Minimal systemic absorption β very safe in liver disease |
| Evidence | Reduces HE recurrence by ~58% vs placebo |
| Precipitant | Treatment |
|---|---|
| GI bleed | β Already treated (band ligation done) |
| Infection | β Ceftriaxone already running |
| Constipation | β Lactulose will address this |
| Electrolyte imbalance | Check KβΊ, NaβΊ, correct if needed |
| Dehydration | Careful IV fluids |
| Drug | Why Avoid |
|---|---|
| Benzodiazepines | Dramatically worsen HE - enhance GABA β more sedation β deeper coma |
| Opioids | CNS depressants - worsen encephalopathy |
| Sedatives/Antihistamines | Same reason |
| Protein restriction | Old teaching - NOW OUTDATED. Actually maintain adequate nutrition - protein restriction worsens outcomes |
β οΈ Classic exam trap: Nurses may want to give Lorazepam for his agitation. As the pharmacist you must intervene - NO benzodiazepines in HE.
| Option | Recommendation |
|---|---|
| Benzodiazepines | π΄ Absolutely avoid |
| Haloperidol (small dose) | π‘ Can be used cautiously if safety risk, but use minimum dose |
| Physical reassurance | β First line - reorient, calm environment |
| Treat HE itself | β As ammonia falls with Lactulose, agitation will settle |
| Thiamine IV | β Give empirically - alcohol + confusion = always give Thiamine to prevent Wernicke's encephalopathy |
| Detail | |
|---|---|
| Drug | Thiamine (Vitamin B1) |
| Dose | Pabrinex IV (high dose thiamine) - 2 pairs TDS for 3 days, then 1 pair OD |
| Why | Chronic alcohol use = Thiamine deficiency β Wernicke's encephalopathy (confusion + ataxia + eye signs) |
| Rule | In ANY confused alcoholic patient β give IV Thiamine BEFORE glucose |
| Critical point | Giving glucose BEFORE Thiamine can precipitate acute Wernicke's β permanent brain damage |
Confused alcoholic patient
β
ALWAYS: IV Thiamine FIRST
β
THEN: IV Glucose if hypoglycaemic
β
NEVER: Glucose before Thiamine
Hepatic Encephalopathy - Grade 2
PHARMACOLOGICAL:
β
Lactulose 30-50ml Q1-2H until bowels open β then titrate to 2-3 stools/day
β
Rifaximin 550mg BD (add on)
β
IV Pabrinex (Thiamine) - 2 pairs TDS Γ 3 days
β
Continue Ceftriaxone (treat infection precipitant)
β
Correct electrolytes (KβΊ, NaβΊ, MgΒ²βΊ)
AVOID:
π΄ Benzodiazepines
π΄ Opioids
π΄ Sedatives
π΄ Glucose before Thiamine
MONITORING:
- GCS/conscious level hourly
- Ammonia level (repeat in 12-24 hours)
- Blood glucose (hypoglycaemia common in cirrhosis)
- Urine output
- If GCS deteriorates β escalate to ITU, consider intubation
| Point | Remember |
|---|---|
| GI bleed triggers HE | Blood = protein = ammonia load |
| Lactulose target | 2-3 soft stools/day - not diarrhoea |
| Rifaximin | Non-absorbable antibiotic, safe in liver disease |
| NO benzodiazepines | Classic dangerous error in HE |
| Thiamine before glucose | Always in confused alcoholic |
| Protein restriction outdated | Maintain nutrition in HE |
Treatment summary
| Intervention | Detail |
|---|---|
| IV Access | 2x large bore cannulas |
| IV Fluids | Cautious crystalloid - target SBP >90 mmHg |
| Blood transfusion | Transfuse if Hb <70 g/L (restrictive strategy) |
| FFP + Platelets | If coagulopathic (cirrhosis = poor clotting) |
| Oxygen | Maintain SpOβ >95% |
| Catheterise | Monitor urine output |
| Drug | Dose | Duration | Purpose |
|---|---|---|---|
| Terlipressin | 2mg IV Q4H β 1mg Q4H after haemostasis | 5 days | Splanchnic vasoconstriction β reduce portal pressure |
| Ceftriaxone | 1g IV OD | 5-7 days | Infection prophylaxis β reduces mortality |
| Endoscopy | Band ligation | Within 12 hours | Definitive bleed control |
| Drug | Dose | Purpose |
|---|---|---|
| Lactulose | 30-50ml Q1-2H until bowels open β titrate to 2-3 stools/day | Reduce ammonia absorption |
| Rifaximin | 550mg BD | Kill ammonia-producing gut bacteria |
| IV Pabrinex (Thiamine) | 2 pairs TDS Γ 3 days β 1 pair OD | Prevent Wernicke's encephalopathy |
| Electrolyte correction | KβΊ, NaβΊ, MgΒ²βΊ | Correct metabolic triggers of HE |
| Drug | Action | Reason |
|---|---|---|
| Ibuprofen 400mg TDS | π΄ STOPPED permanently | GI bleed, renal risk, worsens portal HTN |
| Metformin 1g BD | π΄ HELD | Haemodynamic instability β lactic acidosis risk |
| Propranolol 40mg BD | π΄ HELD acutely | Masks tachycardia, worsens hypotension in shock |
| Spironolactone 100mg OD | π΄ HELD | AKI risk in haemodynamic shock |
| Drug | When to Restart | Note |
|---|---|---|
| Propranolol | Once haemodynamically stable | Long-term secondary prevention of variceal rebleed |
| Spironolactone | Once renal function stable | Ascites management in cirrhosis |
| Metformin | Once eating, haemodynamically stable, eGFR checked | Consider alternatives given liver disease |
| Option | Recommendation |
|---|---|
| Paracetamol | β Preferred - max 2g/day in cirrhosis (reduced dose) |
| Topical NSAIDs | π‘ Minimal systemic absorption - discuss with team |
| Opioids | π΄ Avoid - worsen HE |
| NSAIDs (oral) | π΄ Permanently contraindicated in cirrhosis |
| Drug Class | Examples | Reason |
|---|---|---|
| Oral NSAIDs | Ibuprofen, Diclofenac, Naproxen | GI bleed, renal failure, hepatorenal syndrome |
| Benzodiazepines | Diazepam, Lorazepam | Precipitate/worsen HE |
| Opioids (routine) | Codeine, Morphine | Worsen HE, precipitate coma |
| Sedatives | Antihistamines, Z-drugs | CNS depression worsens HE |
| Parameter | Frequency | Target |
|---|---|---|
| BP + HR | Every 15 min initially β hourly when stable | SBP >90, HR <100 |
| GCS | Hourly | Improving towards 15 |
| Blood glucose | Q4H | 4-10 mmol/L |
| Ammonia | Daily | Downward trend |
| U&E + Creatinine | Daily | Monitor AKI |
| Hb | 6-12 hourly initially | >70 g/L |
| Stools | Daily count | 2-3 soft stools/day (Lactulose target) |
| LFTs | Every 48 hours | Trend |
| Intervention | Detail |
|---|---|
| Propranolol | Restart - reduces portal pressure, prevents rebleed |
| Lactulose | Continue long term for recurrent HE prevention |
| Rifaximin | Continue long term if recurrent HE |
| Alcohol cessation | Refer to addiction services - most important intervention |
| Thiamine supplementation | Oral Thiamine 100mg OD long term |
| Repeat endoscopy | Band ligation programme until varices eradicated |
| Hepatology follow-up | Monitor for hepatocellular carcinoma (6-monthly USS + AFP) |
| Ibuprofen counselling | Never take OTC NSAIDs again - clearly documented in notes |
| # | Pearl |
|---|---|
| 1 | Ibuprofen in cirrhosis = a prescription for disaster. Always check OTC medications in liver patients |
| 2 | Terlipressin + Ceftriaxone before endoscopy - do not wait for the scope to start drugs |
| 3 | Thiamine BEFORE glucose in any confused alcoholic - non-negotiable |
| 4 | Lactulose target = 2-3 soft stools/day - underdosing is the most common error |
| 5 | Propranolol is good long term for varices but HOLD it in acute shock |
| Area | Performance |
|---|---|
| Identifying variceal bleed | β Correct |
| Recognising Ibuprofen as harmful | β Good catch |
| Engaging with HE management | β Good learning |
| Asking right questions | β Strong throughout |
Let's start with today case
As per the gina 2025 guidelines, this thing is confirmed as asthama , no idea about servity, ibuprofen is problem here must be stopped
Ibuprofen (NSAID) β COX-1 inhibition
β
Arachidonic acid diverted to lipoxygenase pathway
β
Excess leukotriene production (LTC4, LTD4, LTE4)
β
Bronchospasm + airway inflammation
β
Asthma attack triggered/worsened
| Fact | Detail |
|---|---|
| Aspirin/NSAID sensitive asthma | Affects ~10-20% of asthmatics |
| Ibuprofen started | 5 days ago - timeline fits perfectly with this attack |
| Action | π΄ STOP immediately, never rechallenge |
| Alternative for back pain | Paracetamol Β± physiotherapy |
| Document | NSAID sensitivity in allergy/alert section of notes |
| Feature | Moderate | Severe | Life-Threatening | Near Fatal |
|---|---|---|---|---|
| SpOβ | >92% | 92-94% | <92% | Hypoxia despite O2 |
| PEFR | 50-75% | 33-50% | <33% | Cannot perform |
| Speech | Sentences | Phrases | Words only | Silent chest |
| HR | <110 | 110-125 | >125 | Bradycardia |
| RR | <25 | 25-30 | >30 | |
| Accessory muscles | No | Yes | Yes |
| Feature | Mrs. Zara | Severity |
|---|---|---|
| SpOβ | 89% on air | π΄ Life-threatening |
| PEFR | 38% predicted | π Severe |
| Speech | Words only | π΄ Life-threatening |
| HR | 124 bpm | π Severe |
| RR | 32/min | π΄ Life-threatening |
| Feature | Significance |
|---|---|
| Silent chest | No wheeze = no air movement = very dangerous |
| Cyanosis | Severe hypoxia |
| Exhaustion/confusion | Impending respiratory failure |
| Hypotension | Cardiovascular compromise |
| PaCOβ normal or high | In severe asthma COβ should be LOW (hyperventilating) - normal/high COβ = tiring, near arrest |
β οΈ Critical point: In asthma, a normal COβ (4.5-6 kPa) is actually alarming - it means the patient is exhausted and can no longer hyperventilate. Immediate escalation needed.
| Detail | |
|---|---|
| Target SpOβ | 94-98% (NOT 100% - hyperoxia can be harmful) |
| Delivery | High flow via non-rebreather mask initially |
| Current | 93% on 15L - marginally acceptable, needs improvement |
| Drug | Dose | Route | Frequency |
|---|---|---|---|
| Salbutamol | 5mg nebulised | Nebuliser driven by Oβ | Every 15-20 min initially, then hourly |
| Ipratropium bromide | 0.5mg nebulised | Add to Salbutamol neb | Every 4-6 hours (first 24 hours) |
Why add Ipratropium? In life-threatening asthma, combining Salbutamol (Ξ²2 agonist) + Ipratropium (anticholinergic) gives greater bronchodilation than either alone. GINA 2025 recommends this combination in severe/life-threatening attacks.
| Drug | Dose | Route | Duration |
|---|---|---|---|
| Prednisolone | 40-50mg OD | Oral (if can swallow) | 5 days |
| Hydrocortisone | 100mg QDS | IV (if cannot swallow/vomiting) | Until oral tolerated |
Steroids take 4-6 hours to work - give them NOW, do not delay.
| Detail | |
|---|---|
| Drug | Magnesium Sulphate |
| Dose | 2g IV over 20 minutes (single dose) |
| Indication | Life-threatening asthma OR poor response to initial bronchodilators |
| Mechanism | Smooth muscle relaxation β bronchodilation |
| Evidence | GINA 2025 + BTS recommend in life-threatening asthma |
| Monitor | BP during infusion (can cause hypotension) |
| Drug | Action | Reason |
|---|---|---|
| Ibuprofen | π΄ STOP permanently | Triggered this attack |
| Salbutamol PRN | β Continue - now via nebuliser | Increase frequency |
| Beclometasone inhaler | π‘ Continue but ineffective acutely | Inhaled steroids - not acute relief |
| Montelukast | β Continue | Leukotriene receptor antagonist - actually helpful here |
| Omeprazole | β Continue | GORD can worsen asthma - keep controlled |
| Drug | Reason |
|---|---|
| NSAIDs/Aspirin | Bronchospasm via leukotriene pathway |
| Beta-blockers (oral or eye drops) | Bronchoconstriction - even topical timolol eye drops! |
| ACE inhibitors | Cough can worsen asthma symptoms |
| Carbachol/Pilocarpine | Cholinergic β bronchospasm |
Mrs. Zara - Life-Threatening Asthma
IMMEDIATE:
β
High flow Oβ β target SpOβ 94-98%
β
Salbutamol 5mg nebulised (Oβ-driven) - back to back initially
β
Ipratropium 0.5mg nebulised - add to Salbutamol
β
Hydrocortisone 100mg IV QDS (or Prednisolone 50mg oral)
β
Magnesium Sulphate 2g IV over 20 minutes
β
STOP Ibuprofen immediately
β
Inform senior/ITU - life-threatening attack
β
ABG - check COβ level urgently
β
CXR - rule out pneumothorax
MONITORING:
- SpOβ continuous
- PEFR every 15-30 minutes (target improvement >50%)
- HR, RR every 15 minutes
- Repeat ABG in 1 hour if not improving
| Point | Remember |
|---|---|
| PEFR 38% + words only + SpOβ 89% | = Life-threatening asthma |
| Normal COβ in severe asthma | Alarming sign - patient tiring |
| Ipratropium | Add in severe/life-threatening only |
| Magnesium Sulphate | 2g IV - for life-threatening attacks |
| Ibuprofen β asthma | NSAIDs trigger attacks in ~10-20% asthmatics |
| Steroids take 4-6 hours | Give early, do not delay |
I think we should intubated, as patient is not responding to steroid I think it's type 1 asthama
| What You May Mean | Correct Term |
|---|---|
| Type 1 / Type 2 respiratory failure | ABG classification of respiratory failure |
| Aspirin-sensitive asthma | NSAID-exacerbated respiratory disease |
| Brittle asthma | Rare, refractory severe asthma |
| Type 1 RF | Type 2 RF | |
|---|---|---|
| PaOβ | LOW (<8 kPa) | LOW (<8 kPa) |
| PaCOβ | LOW or NORMAL | HIGH (>6 kPa) |
| Mechanism | V/Q mismatch - lungs failing to oxygenate | Ventilatory failure - can't breathe out COβ |
| In asthma | Early/moderate attack | Late/severe - patient tiring |
| Significance | Serious | Near fatal - intubate |
| Parameter | Result | Normal | Flag |
|---|---|---|---|
| pH | 7.31 | 7.35-7.45 | π΄ Acidotic |
| PaOβ | 7.2 kPa | >10 kPa | π΄ LOW |
| PaCOβ | 6.8 kPa | 4.5-6.0 kPa | π΄ RISING |
| HCOβ | 22 mmol/L | 22-26 | Normal |
| Lactate | 2.1 mmol/L | <2.0 | π‘ Mildly raised |
| Indication | Present in Mrs. Zara? |
|---|---|
| Rising PaCOβ / Type 2 RF | β Yes - PaCOβ 6.8 |
| Falling pH (acidosis) | β Yes - pH 7.31 |
| Exhaustion / silent chest | β Assess now |
| SpOβ not improving | β Still 91% |
| Falling GCS | β Check |
| Failed medical management (1 hour) | β Yes |
| Detail | |
|---|---|
| Drug | Salbutamol IV |
| Dose | 250mcg slow IV bolus then 5-20 mcg/min infusion |
| When | Nebulised route failing - IV gives direct systemic effect |
| Monitor | HR, KβΊ (salbutamol causes hypokalaemia) |
| GINA 2025 | Recommends IV salbutamol when inhaled therapy insufficient |
| Detail | |
|---|---|
| Drug | Aminophylline IV |
| Dose | 5mg/kg loading dose over 20 min (if not on theophylline) then 0.5mg/kg/hr infusion |
| Mechanism | Phosphodiesterase inhibitor β bronchodilation |
| Caution | Narrow therapeutic index - check level, monitor ECG |
| Caution | If already on oral Theophylline β DO NOT give loading dose (toxicity risk) |
| Detail | |
|---|---|
| What | Helium-Oxygen mixture (70:30 or 80:20) |
| Mechanism | Lower density gas β less turbulent airflow β easier breathing |
| Use | Buys time before intubation |
| Availability | Not all centres have it |
| Drug | Recommendation | Reason |
|---|---|---|
| Ketamine | β PREFERRED induction agent | Causes bronchodilation - unique advantage in asthma |
| Propofol | π‘ Acceptable | Neutral on airways |
| Thiopentone | π΄ Avoid | Can trigger histamine release β worsen bronchospasm |
| Suxamethonium | π‘ Use with caution | Check KβΊ first - salbutamol already lowering KβΊ |
| Rocuronium | β Preferred paralytic | No histamine release |
| Morphine | π΄ Avoid pre-intubation | Histamine release β worsen bronchospasm |
| Fentanyl | β Use instead of morphine | No histamine release |
β οΈ Note: Ketamine is PREFERRED in asthma intubation - opposite of SAH where we avoided it! Context determines drug choice.
| Parameter | Standard Ventilation | Asthma Strategy |
|---|---|---|
| RR | 12-16/min | 6-10/min (low) |
| Tidal Volume | 8-10 ml/kg | 6-8 ml/kg (low) |
| I:E ratio | 1:2 | 1:3 or 1:4 (long expiratory) |
| PaCOβ target | 4.5-6 kPa | Allow up to 8-10 kPa |
| Why | Asthma = air trapping - need long expiratory time to empty lungs |
Permissive hypercapnia = deliberately allowing COβ to rise to avoid barotrauma from high airway pressures. Lower rate + longer expiration = lungs can empty properly.
| Drug | Detail |
|---|---|
| Continue nebulised Salbutamol | Via inline nebuliser on ventilator circuit |
| Continue IV corticosteroids | Hydrocortisone 100mg QDS |
| Sedation | Propofol or Midazolam - keep sedated to prevent fighting ventilator |
| Ketamine infusion | Can continue post-intubation - bronchodilatory benefit |
| Monitor KβΊ | Salbutamol + steroids both cause hypokalaemia - replace aggressively |
| Replace KβΊ | Target KβΊ >4.0 mmol/L in ventilated asthma patient |
Hour 1 - Not improving β Escalate:
STEP 1 (Next 15 minutes):
β
IV Salbutamol 250mcg bolus β infusion
β
IV Aminophylline (if not on theophylline)
β
Call ITU NOW - do not delay
β
Repeat ABG
STEP 2 (If no improvement / Type 2 RF confirmed):
β
RSI with Ketamine + Rocuronium + Fentanyl
β
Avoid Thiopentone, Morphine, Suxamethonium
β
Post-intubation: permissive hypercapnia strategy
β
Continue Salbutamol nebs via ventilator
β
Monitor KβΊ aggressively - replace to >4.0
STOP PERMANENTLY:
π΄ Ibuprofen - document NSAID sensitivity
π΄ Any future NSAIDs or Aspirin
| Point | Remember |
|---|---|
| Type 2 RF in asthma | Rising COβ = patient tiring = near fatal |
| Ketamine in asthma RSI | PREFERRED - bronchodilator |
| Avoid Thiopentone/Morphine | Histamine release worsens bronchospasm |
| Permissive hypercapnia | Low RR, long expiration, allow COβ to rise |
| KβΊ monitoring | Salbutamol + steroids = hypokalaemia risk |
| IV Salbutamol | Try before intubating |
| "Type 1/2 Asthma" | Not a real classification - know RF types instead |
I have some doubt , what should be rass score here
| Score | Label | Description |
|---|---|---|
| +4 | Combative | Violent, immediate danger to staff |
| +3 | Very Agitated | Pulls/removes tubes, aggressive |
| +2 | Agitated | Frequent non-purposeful movement, fights ventilator |
| +1 | Restless | Anxious, movements not aggressive |
| 0 | Alert & Calm | Normal awake state |
| -1 | Drowsy | Not fully alert, sustained awakening to voice (>10 sec) |
| -2 | Light Sedation | Briefly awakens to voice (<10 sec) |
| -3 | Moderate Sedation | Movement to voice, no eye contact |
| -4 | Deep Sedation | No response to voice, moves to physical stimulation |
| -5 | Unarousable | No response to voice OR physical stimulation |
No sedation needed yet - she is not intubated. Agitation is appropriate - it is her respiratory distress driving it.
| Target | RASS Score | Reason |
|---|---|---|
| Initial post-intubation | -2 to -3 | Deep enough to tolerate ETT, stop fighting ventilator |
| First 24-48 hours | -2 to -3 | Severe bronchospasm - need to minimise airway stimulation |
| Stabilising phase | -1 to -2 | Light sedation as bronchospasm improves |
| Weaning phase | 0 to -1 | Wake up, assess for extubation |
| Drug | Dose | RASS Target | Notes |
|---|---|---|---|
| Propofol | 0.5-4 mg/kg/hr IV infusion | -2 to -3 | β Titratable, quick offset, preferred in ITU |
| Midazolam | 0.02-0.1 mg/kg/hr | -2 to -3 | π‘ Longer acting, accumulates in liver disease |
| Ketamine infusion | 0.1-0.5 mg/kg/hr | -2 to -3 | β Double benefit - sedation + bronchodilation |
| Fentanyl infusion | 25-100 mcg/hr | Analgesia | β No histamine release - safe in asthma |
| Drug | Reason |
|---|---|
| Morphine infusion | Histamine release β worsens bronchospasm |
| Deep RASS -5 unnecessarily | Over-sedation β ICU weakness, delayed weaning |
Every morning on ITU ward round:
1. Check current RASS score
β
2. Is patient at target RASS?
β
3. Daily sedation hold (SAT - Spontaneous Awakening Trial)
β Reduce/stop sedation
β Reassess RASS
β
4. If RASS reaches 0 to -1 and stable:
β Spontaneous Breathing Trial (SBT)
β Consider extubation
β
5. If patient agitated (+1 or above):
β Reassess pain first (CPOT score)
β Retitrate sedation
| Tool | Purpose |
|---|---|
| RASS | Measures sedation/agitation level |
| CAM-ICU | Screens for delirium in ICU patients |
| Used together | RASS first β if RASS -3 or better β do CAM-ICU |
As a clinical pharmacist on ITU, you should be checking RASS + CAM-ICU daily and reviewing sedation appropriateness.
Timeline:
Pre-intubation now:
RASS +1 to +2 (distressed, no sedation needed yet)
β
Immediately post-intubation (first 24-48 hours):
Target RASS -2 to -3
Drugs: Propofol + Ketamine infusion + Fentanyl
β
Bronchospasm improving (Day 2-3):
Target RASS -1 to -2
Reduce sedation slowly
β
Weaning phase:
Target RASS 0 to -1
Daily sedation hold β SBT β extubation if ready
| Point | Remember |
|---|---|
| RASS 0 = normal awake | Not sedated, not agitated |
| Post-intubation asthma target | -2 to -3 initially |
| Propofol + Ketamine | Ideal combination in ventilated asthma |
| Avoid morphine infusion | Histamine release in asthma |
| Daily sedation hold | Best practice - reduces ITU stay |
| Pain before sedation | Always treat pain first (analgesia first model) |
| RASS before CAM-ICU | Cannot assess delirium if too deeply sedated |
New case pls
It's diabetic ketoacidosis, does he have burning sensation while urination, what's his potasium level
β This confirms a urinary tract infection (UTI) as the likely precipitant of his DKA
| Test | Result | Normal | Flag |
|---|---|---|---|
| Potassium (KβΊ) | 6.1 mmol/L | 3.5-5.0 | π΄ HIGH |
| Sodium (NaβΊ) | 131 mmol/L | 135-145 | π‘ LOW |
| Bicarbonate (HCOβ) | 8 mmol/L | 22-26 | π΄ CRITICALLY LOW |
| pH (VBG) | 7.18 | 7.35-7.45 | π΄ ACIDOTIC |
| Urea | 13.4 mmol/L | 2.5-7.8 | π΄ HIGH |
| Creatinine | 168 Β΅mol/L | 60-110 | π΄ HIGH |
| eGFR | 42 mL/min | >60 | π΄ LOW |
| WBC | 18.2 Γ 10βΉ/L | 4-11 | π΄ HIGH |
| CRP | 142 mg/L | <5 | π΄ HIGH |
| Lactate | 2.8 mmol/L | <2.0 | π΄ HIGH |
| Criterion | Threshold | Mr. Hassan |
|---|---|---|
| Blood glucose | >11 mmol/L | β 28.4 mmol/L |
| Blood ketones | >3 mmol/L | β 5.8 mmol/L |
| Bicarbonate | <15 mmol/L OR pH <7.3 | β HCOβ 8, pH 7.18 |
| Severity | pH | Bicarbonate | Ketones |
|---|---|---|---|
| Mild | 7.25-7.30 | 15-18 | >3 |
| Moderate | 7.00-7.24 | 10-14 | >3 |
| Severe | <7.00 | <10 | >3 |
Insulin deficiency + acidosis in DKA
β
HβΊ ions move INTO cells
β
KβΊ shifts OUT of cells into bloodstream
β
Serum KβΊ appears HIGH
β
BUT total body potassium is actually DEPLETED
(lost through vomiting + osmotic diuresis)
| Phase | KβΊ Behaviour | Risk |
|---|---|---|
| On admission | HIGH (6.1) - due to shift | Hyperkalaemia β cardiac arrhythmia |
| After insulin started | Rapidly FALLS | KβΊ shifts back into cells |
| If not replaced | Can drop to dangerously LOW | Hypokalaemia β fatal arrhythmia |
| Time | Fluid | Rate | Reason |
|---|---|---|---|
| 0-60 min | 0.9% NaCl 1L | Over 1 hour | Resuscitation - he is hypotensive |
| 1-2 hours | 0.9% NaCl 1L | Over 1 hour | Continued rehydration |
| 2-4 hours | 0.9% NaCl 1L | Over 2 hours | Rehydration |
| 4-8 hours | 0.9% NaCl 1L | Over 4 hours | Maintenance |
| 8-12 hours | 0.9% NaCl 1L | Over 4 hours | Maintenance |
When glucose falls to <14 mmol/L β switch to 10% Dextrose alongside saline to prevent hypoglycaemia while continuing insulin
| Rule | Detail |
|---|---|
| Check KβΊ BEFORE starting insulin | β Done - KβΊ 6.1 |
| If KβΊ <3.5 | Do NOT start insulin - replace KβΊ first, insulin will drop it further |
| If KβΊ 3.5-5.5 | Start insulin + add KCl to fluids |
| If KβΊ >5.5 | β Start insulin WITHOUT KβΊ replacement yet - insulin will bring KβΊ down |
| Drug | Dose | Route |
|---|---|---|
| Fixed rate insulin infusion (FRIII) | 0.1 units/kg/hour | IV infusion |
| Mr. Hassan (approx 80kg) | 8 units/hour | IV |
| Continue until | Ketones <0.3 + pH >7.3 + eating | Then switch to SC |
β οΈ Do NOT stop background Glargine (Lantus) - continue 24 units nocte throughout DKA treatment. Common error to stop it!
| KβΊ Level | Action |
|---|---|
| >5.5 | No KβΊ replacement (Mr. Hassan now) |
| 3.5-5.5 | Add 40mmol KCl per litre of IV fluid |
| <3.5 | Stop insulin, urgent KβΊ replacement, senior review |
| Drug | Dose | Duration | Reason |
|---|---|---|---|
| IV Co-amoxiclav 1.2g TDS | TDS | 5-7 days | UTI precipitated DKA - treat aggressively |
| Or IV Ceftriaxone 1g OD | OD | 5-7 days | If penicillin allergy |
| Send MSU | Urine culture | Before antibiotics | Guide definitive therapy |
| Drug | Action | Reason |
|---|---|---|
| Ramipril | π΄ Hold | AKI (creatinine 168, eGFR 42) + hypotension |
| Sertraline | π‘ Continue with caution | Check QTc - SSRIs can prolong QT, monitor ECG |
| Paracetamol | β Continue PRN | Safe, useful for fever from UTI |
| Insulin Glargine | β Continue nocte | Do NOT stop background insulin |
| Insulin Aspart | π΄ Hold meal doses | Replaced by FRIII during DKA |
| Parameter | Frequency | Target |
|---|---|---|
| Blood glucose | Hourly | Falling by 3-4 mmol/L per hour |
| Blood ketones | Hourly | Falling by 0.5 mmol/L per hour |
| KβΊ | Every 1-2 hours | 4.0-5.5 mmol/L |
| pH/VBG | 2 hourly | Rising towards 7.35 |
| BP, HR | Every 30 min initially | SBP >100, HR <100 |
| Urine output | Hourly (catheterise) | >0.5 ml/kg/hour |
| GCS | Hourly | Improving |
| Point | Remember |
|---|---|
| KβΊ high on admission but depleted | Most dangerous aspect of DKA |
| Check KβΊ before insulin | If <3.5 β replace first, do not start insulin |
| KβΊ >5.5 β no replacement yet | Insulin will bring it down |
| Never stop Glargine | Continue background insulin throughout |
| Glucose <14 β add 10% dextrose | Prevents hypoglycaemia while insulin continues |
| UTI = classic DKA precipitant | Treat aggressively with IV antibiotics |
| Ramipril hold in AKI | Restart once renal function recovers |
Can you present me glucose reading in mg/dl, abg value in mmhg
| mmol/L | mg/dL | |
|---|---|---|
| Admission glucose | 28.4 mmol/L | 511 mg/dL |
| DKA threshold | >11 mmol/L | >198 mg/dL |
| Switch to dextrose when | <14 mmol/L | <252 mg/dL |
| Normal fasting | 4-7 mmol/L | 72-126 mg/dL |
Conversion formula: mmol/L Γ 18 = mg/dL
| Parameter | Original | Converted | Normal Range |
|---|---|---|---|
| pH | 7.18 | 7.18 (no conversion needed) | 7.35-7.45 π΄ |
| PaOβ | - | Not measured (VBG) | >80 mmHg |
| PaCOβ | Low (compensatory) | ~25-28 mmHg | 35-45 mmHg π΄ LOW |
| HCOβ | 8 mmol/L | 8 mEq/L (same value) | 22-26 mEq/L π΄ |
| Lactate | 2.8 mmol/L | 25.2 mg/dL | <18 mg/dL π΄ |
Metabolic acidosis (HCOβ = 8)
β
Body tries to compensate
β
Increases respiratory rate (RR 26/min)
β
Blows off COβ
β
PaCOβ drops to ~25-28 mmHg
β
This is Kussmaul breathing
(deep, sighing respirations noted on admission)
| Feature | What It Means |
|---|---|
| Kussmaul breathing | Deep sighing respirations - body compensating for metabolic acidosis |
| Low PaCOβ | Respiratory compensation - good sign body is trying |
| Fruity breath | Acetone from ketone breakdown - classic DKA sign |
| Parameter | Normal | Mr. Hassan | Unit | Interpretation |
|---|---|---|---|---|
| pH | 7.35-7.45 | 7.18 | - | π΄ Severe acidosis |
| PaOβ | 80-100 | Not measured | mmHg | VBG used |
| PaCOβ | 35-45 | ~26 | mmHg | π΄ Low - respiratory compensation |
| HCOβ | 22-26 | 8 | mEq/L | π΄ Critically low |
| SpOβ | 95-100% | 97% | % | β Normal |
| Lactate | <2.0 | 2.8 (=25 mg/dL) | mmol/L | π΄ Mildly elevated |
| Ketones | <0.6 | 5.8 | mmol/L | π΄ Severely elevated |
| Measurement | Formula |
|---|---|
| Glucose mmol/L β mg/dL | Γ 18 |
| Glucose mg/dL β mmol/L | Γ· 18 |
| Lactate mmol/L β mg/dL | Γ 9 |
| PaCOβ kPa β mmHg | Γ 7.5 |
| PaOβ kPa β mmHg | Γ 7.5 |
| HCOβ | Same value in mmol/L and mEq/L |
In such case we have to re check blood glucose, and to decide weather insulin should be stopped or not , stat or admin kcl infusion
KβΊ drops to 3.1 mmol/L during insulin infusion
β
KβΊ < 3.5 mmol/L threshold reached
β
STOP insulin infusion IMMEDIATELY
β
START urgent KCl replacement
β
Recheck KβΊ after 1 hour
β
Once KβΊ > 3.5 β restart insulin
| KβΊ Level | Action |
|---|---|
| >5.5 mmol/L | No KCl - insulin only |
| 3.5-5.5 mmol/L | Add 40mmol KCl per litre of IV fluid |
| <3.5 mmol/L | STOP insulin + urgent KCl replacement |
| <2.5 mmol/L | Emergency - cardiac monitoring, senior review immediately |
| Detail | |
|---|---|
| Concentration | 40mmol KCl in 1L 0.9% NaCl |
| Rate | Over 1 hour (max safe rate = 20mmol/hour peripherally) |
| Route | Peripheral IV acceptable at this concentration |
| Monitoring | Continuous cardiac monitoring (ECG) during infusion |
| Recheck KβΊ | After 1 hour |
β οΈ Never give KCl as IV bolus - fatal cardiac arrhythmia. Always diluted, always infusion.
| Reason | Detail |
|---|---|
| Glucose may have dropped to <14 mmol/L (252 mg/dL) | Time to add 10% dextrose alongside saline |
| Hypoglycaemia risk | Insulin running for 3 hours - glucose may be falling fast |
| DKA resolution check | Is ketone clearance on track? |
| Parameter | Admission | Expected Hour 3 | Target Rate |
|---|---|---|---|
| Glucose | 511 mg/dL (28.4) | ~350-400 mg/dL (~20-22 mmol/L) | Fall 3-4 mmol/L per hour |
| Ketones | 5.8 mmol/L | ~4.3-4.8 mmol/L | Fall 0.5 mmol/L per hour |
Hour 3 results:
KβΊ = 3.1 mmol/L β STOP insulin NOW
β Start KCl 40mmol in 1L NaCl over 1 hour
β ECG monitoring
Recheck glucose:
β If glucose >14 mmol/L (>252): continue saline, restart insulin once KβΊ >3.5
β If glucose <14 mmol/L (<252): add 10% dextrose 125ml/hr alongside saline
β If glucose <4 mmol/L (<72): treat hypoglycaemia - 150ml 10% dextrose bolus
After 1 hour - recheck KβΊ:
β KβΊ >3.5 β restart insulin infusion 0.1 units/kg/hr
β KβΊ still <3.5 β continue KCl, do not restart insulin yet
β KβΊ <2.5 β emergency, escalate to senior immediately
| KβΊ Level | ECG Changes |
|---|---|
| 3.1-3.5 | Flat/inverted T waves, U waves appearing |
| 2.5-3.0 | Prominent U waves, ST depression |
| <2.5 | Widened QRS, VT/VF risk |
Pharmacist role: Flag KβΊ to nurse and doctor immediately, ensure cardiac monitoring is on, ensure KCl is prescribed correctly (right concentration, right rate).
| Rule | Detail |
|---|---|
| 1 | Always check KβΊ before starting insulin |
| 2 | KβΊ <3.5 = STOP insulin, replace first |
| 3 | KβΊ 3.5-5.5 = insulin + 40mmol KCl per litre |
| 4 | KβΊ >5.5 = insulin only, no KCl yet |
| 5 | Recheck KβΊ every hour during active DKA |
| 6 | Never bolus KCl - always diluted infusion |
| 7 | Cardiac monitoring during KCl replacement |
Complete treatment summary in soap format
| Drug | Dose | Frequency | Concerns |
|---|---|---|---|
| Insulin Glargine (Lantus) | 24 units | SC nocte | Continue throughout DKA |
| Insulin Aspart (NovoRapid) | Variable | With meals | Hold - replaced by FRIII |
| Ramipril | 5mg | OD | Hold - AKI + hypotension |
| Sertraline | 100mg | OD | Continue - monitor QTc |
| Paracetamol | 1g | QDS PRN | Continue - safe, useful for fever |
| Parameter | Value | Normal | Flag |
|---|---|---|---|
| BP | 98/62 mmHg | 120/80 | π΄ Hypotensive |
| HR | 114 bpm | 60-100 | π΄ Tachycardia |
| RR | 26/min (Kussmaul) | 12-20 | π΄ High |
| Temp | 38.2Β°C | 36.5-37.5 | π‘ Febrile |
| SpOβ | 97% on air | >95% | β |
| GCS | 13/15 | 15 | π΄ Reduced |
| Breath | Fruity/acetone odour | - | π΄ Ketosis |
| Test | Result | Normal | Flag |
|---|---|---|---|
| Blood glucose | 511 mg/dL (28.4 mmol/L) | 72-126 mg/dL | π΄ |
| Blood ketones | 5.8 mmol/L | <0.6 | π΄ |
| Urine dipstick | Ketones +++, Glucose +++, Leucocytes +, Nitrites + | - | π΄ |
| Test | Result | Normal | Flag |
|---|---|---|---|
| pH (VBG) | 7.18 | 7.35-7.45 | π΄ Severe acidosis |
| PaCOβ | ~26 mmHg | 35-45 mmHg | π΄ Low (compensation) |
| HCOβ | 8 mEq/L | 22-26 | π΄ Critically low |
| KβΊ | 6.1 mmol/L | 3.5-5.0 | π΄ High (transcellular shift) |
| NaβΊ | 131 mmol/L | 135-145 | π‘ Low |
| Urea | 13.4 mmol/L | 2.5-7.8 | π΄ High |
| Creatinine | 168 Β΅mol/L | 60-110 | π΄ High (AKI) |
| eGFR | 42 mL/min | >60 | π΄ Low |
| WBC | 18.2 Γ 10βΉ/L | 4-11 | π΄ Infection |
| CRP | 142 mg/L | <5 | π΄ Infection |
| Lactate | 2.8 mmol/L (25 mg/dL) | <2.0 | π΄ Elevated |
| Criterion | Mr. Hassan | Severity Marker |
|---|---|---|
| pH 7.18 | <7.00 threshold | π΄ Severe |
| HCOβ 8 mEq/L | <10 threshold | π΄ Severe |
| Ketones 5.8 mmol/L | >3 mmol/L | π΄ Severe |
Insulin deficiency + infection (counter-regulatory hormones)
β
Uncontrolled lipolysis β ketone production
Uncontrolled gluconeogenesis β hyperglycaemia
β
Osmotic diuresis β dehydration β AKI
Ketone accumulation β metabolic acidosis
KβΊ shifts extracellularly β apparent hyperkalaemia
β
Severe DKA: pH 7.18, HCOβ 8, ketones 5.8
| # | Problem | Drug | Severity |
|---|---|---|---|
| 1 | AKI + hypotension | Ramipril - hold | π΄ High |
| 2 | Meal insulin not appropriate during DKA | Insulin Aspart - hold, replace with FRIII | π΄ High |
| 3 | Background insulin must continue | Glargine - do NOT stop | π΄ High |
| 4 | QTc monitoring needed | Sertraline (SSRI) in acutely unwell patient | π‘ Medium |
| 5 | Hypokalaemia risk | Insulin infusion drives KβΊ into cells | π΄ High |
| 6 | UTI precipitant untreated | Start IV antibiotics | π΄ High |
| Time | Fluid | Rate | Rationale |
|---|---|---|---|
| 0-1 hr | 0.9% NaCl 1L | Over 1 hour | Shocked - BP 98/62 |
| 1-2 hr | 0.9% NaCl 1L | Over 1 hour | Continue resuscitation |
| 2-4 hr | 0.9% NaCl 1L | Over 2 hours | Rehydration |
| 4-8 hr | 0.9% NaCl 1L | Over 4 hours | Maintenance |
| 8-12 hr | 0.9% NaCl 1L | Over 4 hours | Maintenance |
| When glucose <252 mg/dL (<14 mmol/L) | Add 10% Dextrose 125ml/hr | Alongside saline | Prevent hypoglycaemia while insulin continues |
| Drug | Dose | Route | Condition |
|---|---|---|---|
| Fixed Rate Insulin Infusion (FRIII) | 0.1 units/kg/hr = 8 units/hr | IV infusion | Start after confirming KβΊ >3.5 |
| Insulin Glargine (Lantus) | 24 units SC nocte | SC | Continue - do NOT stop |
| Insulin Aspart (NovoRapid) | Hold | - | Resume when eating and DKA resolved |
| KβΊ Level | Action |
|---|---|
| >5.5 (admission 6.1) | Insulin only, no KCl - insulin will reduce KβΊ |
| 3.5-5.5 | Add 40mmol KCl per litre of IV fluid |
| <3.5 (Hour 3: KβΊ 3.1) | STOP insulin + KCl 40mmol in 1L NaCl over 1 hour |
| <2.5 | Emergency - senior review, cardiac monitoring |
| Drug | Dose | Route | Duration |
|---|---|---|---|
| IV Co-amoxiclav | 1.2g TDS | IV | 5-7 days (step down to oral when tolerating) |
| If penicillin allergy | Ceftriaxone 1g OD IV | IV | 5-7 days |
| Send MSU | Before first dose | - | Guide de-escalation |
| Drug | Decision | Reason | When to Restart |
|---|---|---|---|
| Ramipril 5mg | π΄ HOLD | AKI (eGFR 42) + hypotension | Once eGFR recovering + BP stable |
| Insulin Aspart | π΄ HOLD | FRIII in place | Resume when eating + DKA resolved |
| Insulin Glargine | β CONTINUE | Prevents rebound ketosis | Throughout admission |
| Sertraline 100mg | β CONTINUE with monitoring | Check QTc on ECG | Continue |
| Paracetamol 1g QDS | β CONTINUE | Fever management, safe | Continue |
| Parameter | Frequency | Target |
|---|---|---|
| Blood glucose | Hourly | Fall 54-72 mg/dL per hour |
| Blood ketones | Hourly | Fall 0.5 mmol/L per hour |
| KβΊ | Every 1-2 hours | 4.0-5.5 mmol/L |
| VBG (pH, HCOβ) | Every 2 hours | pH rising toward 7.35 |
| BP + HR | Every 30 min initially | SBP >100, HR <100 |
| Urine output | Hourly (catheterise) | >0.5 ml/kg/hour |
| GCS | Hourly | Improving to 15 |
| ECG | On admission + during KCl | QTc, KβΊ changes |
| Temperature | Every 4 hours | Trending down with antibiotics |
| Topic | Key Message |
|---|---|
| Sick day rules | Never stop insulin when unwell - increase monitoring instead |
| UTI recognition | Seek treatment early - infection triggers DKA |
| Ketone monitoring | Check ketones when glucose >250 mg/dL (14 mmol/L) |
| Insulin technique | Review injection sites, storage, technique |
| Alcohol + missed doses | Address adherence concerns |
| Ramipril restart | Explain why held, confirm follow-up bloods |
| Diabetes specialist nurse | Refer before discharge |
| Area | Performance |
|---|---|
| DKA diagnosis | β Immediate and correct |
| Asking about UTI symptoms | β Excellent clinical thinking |
| Requesting KβΊ first | β Critical safety step |
| KβΊ management at Hour 3 | β Correct approach - refined with protocol |
| SOAP format requested | β Professional documentation skill |
Next case
"ST elevation of 3mm in leads II, III, aVF. Reciprocal ST depression in leads I and aVL. Normal sinus rhythm. No bundle branch block."
I think we are going in a wrong way , I am clinical pharmacist not physian, I think we are moving towards physian side
| Pharmacist Role | Examples |
|---|---|
| Medication reconciliation | What is the patient on? What needs changing? |
| Drug interactions | Identify dangerous combinations |
| Dose optimisation | Right drug, right dose, right route for this patient |
| Contraindications | Flag drugs that should not be used |
| Renal/hepatic dose adjustment | Adjust for organ dysfunction |
| Therapeutic drug monitoring | Levels, timing, interpretation |
| Adverse drug reaction identification | Is this symptom drug-related? |
| Antibiotic stewardship | Right antibiotic, right duration, de-escalation |
| Counselling | Patient education on new medications |
| Pharmacoeconomics | Cost-effective prescribing |
"Dr. Afzal, the diagnosis is Inferior STEMI. We are activating the cath lab for primary PCI. Can you please review his medications and advise on the pharmacological management from your end?"
| Drug | Your Pharmacist Question |
|---|---|
| Aspirin 75mg OD (already on) | Does he need a loading dose? What about a second antiplatelet? |
| Metformin 1g BD | Safe to continue peri-PCI? |
| Atorvastatin 20mg ON | Is this the right dose for a STEMI patient? |
| Losartan 50mg OD | Any role acutely? Any concerns? |
| Amlodipine 10mg OD | Any concerns in acute MI? |
| Allopurinol 100mg OD | Any interactions with new drugs being added? |
Nope 1 Aspirin 300 mg 2 add clopidrogel 300 my For metformin and atorcastatin I need info on egfr and sr creatinine
| Detail | |
|---|---|
| Why 300mg? | Loading dose needed even though already on 75mg maintenance |
| Mechanism | Irreversible COX-1 inhibition β antiplatelet effect |
| Route | Oral (chewed for faster absorption) or dispersible |
| Then | Continue 75mg OD lifelong post-STEMI |
| Drug | Loading Dose | Maintenance | Note |
|---|---|---|---|
| Clopidogrel | 300mg (or 600mg pre-PCI) | 75mg OD Γ 12 months | β Your answer |
| Ticagrelor | 180mg | 90mg BD Γ 12 months | β Preferred by ESC/NICE in STEMI |
| Prasugrel | 60mg | 10mg OD Γ 12 months | β Alternative - avoid if >75yrs, <60kg, stroke history |
Current ESC 2023 STEMI guidelines prefer Ticagrelor over Clopidogrel for STEMI going to PCI - stronger, faster antiplatelet effect. Clopidogrel is acceptable but second choice unless Ticagrelor contraindicated.
| Test | Result | Normal | Flag |
|---|---|---|---|
| Creatinine | 142 Β΅mol/L | 60-110 | π΄ HIGH (raised from baseline 115) |
| eGFR | 48 mL/min/1.73mΒ² | >60 | π΄ LOW |
| Urea | 9.2 mmol/L | 2.5-7.8 | π‘ Mildly high |
| NaβΊ | 138 mmol/L | 135-145 | β Normal |
| KβΊ | 4.2 mmol/L | 3.5-5.0 | β Normal |
| HbA1c | 8.4% | <6.5% | π΄ Poorly controlled DM |
| Total Cholesterol | 5.8 mmol/L | <5.0 | π΄ High |
| LDL | 3.6 mmol/L | <1.8 in high risk | π΄ High |
| Troponin I | 2,840 ng/L | <52 ng/L | π΄ Significantly elevated |
Inthink we should stop metformin here, with elevated creatinine I can't allow to inc atorcastatin dose so can we switch to Rosuvastatin 20 mg
| Reason | Detail |
|---|---|
| eGFR 48 | Already borderline - stop at eGFR <45 routinely |
| Acute MI + haemodynamic instability | Risk of further AKI - lactic acidosis risk increases |
| Contrast dye for PCI | Contrast nephropathy can acutely worsen renal function |
| Standard protocol | Metformin held 48 hours before and after contrast administration |
| eGFR | Action |
|---|---|
| >45 | Continue |
| 30-45 | Reduce dose, review regularly |
| <30 | Stop permanently |
| Any acute illness + contrast | Stop regardless of baseline eGFR |
| Drug | Use |
|---|---|
| Insulin sliding scale | Acute phase - tight glucose control peri-PCI |
| Target glucose | 6-10 mmol/L (108-180 mg/dL) in ACS |
| Metformin | Restart at discharge if eGFR recovered |
| Statin | Renal Clearance | Dose Adjustment in CKD? |
|---|---|---|
| Atorvastatin | Minimal renal excretion (~2%) | β No dose adjustment needed in CKD |
| Rosuvastatin | ~10% renal excretion | π‘ Caution in severe CKD (eGFR <30) |
| Simvastatin | Minimal renal | No adjustment needed |
Key point: Atorvastatin is actually SAFER in CKD than Rosuvastatin because it has virtually no renal clearance. The concern about creatinine does not limit Atorvastatin dose escalation.
| Situation | Target LDL | Statin Required |
|---|---|---|
| General population | <3.0 mmol/L | Low-moderate intensity |
| High cardiovascular risk | <1.8 mmol/L | High intensity |
| STEMI / Very high CV risk | <1.4 mmol/L | Maximum intensity statin |
| High Intensity Statin | Dose | LDL Reduction |
|---|---|---|
| Atorvastatin | 40-80mg ON | ~50% reduction |
| Rosuvastatin | 20-40mg ON | ~50% reduction |
| Assessment | |
|---|---|
| Rosuvastatin 20mg | β High intensity - acceptable choice |
| Atorvastatin 40-80mg | β Also correct - preferred first line in most guidelines |
| Reasoning (renal concern) | π‘ Not quite right - Atorvastatin is actually safer renally than Rosuvastatin |
| End result | β Switching to high intensity statin is the right action |
Conclusion: Your clinical decision to escalate to high intensity statin is correct. However the reasoning needs refinement - switch to Rosuvastatin is acceptable, but you could equally have just escalated Atorvastatin to 40-80mg which is actually more renal-friendly.
| eGFR | Rosuvastatin Max Dose |
|---|---|
| >30 | Up to 40mg - standard dosing |
| eGFR 30-60 (Mr. Khalid eGFR 48) | Max 20mg - your dose is correct! |
| <30 | Avoid or use with extreme caution |
| Drug | Previous | New Decision | Reason |
|---|---|---|---|
| Aspirin 75mg | Continue | Load 300mg then 75mg OD lifelong | STEMI + PCI |
| Clopidogrel | Not prescribed | Add 300mg load β 75mg OD Γ 12 months | DAPT post-PCI |
| (Consider Ticagrelor 180mg load β 90mg BD) | - | ESC preferred P2Y12 | Discuss with cardiologist |
| Metformin 1g BD | Continue | STOP | AKI risk + contrast PCI |
| Atorvastatin 20mg | Continue | Switch to Rosuvastatin 20mg ON | High intensity needed, dose capped at 20mg for eGFR 48 |
| Losartan 50mg | Continue | Review post-PCI | ARB - beneficial in MI but monitor KβΊ and BP |
| Amlodipine 10mg | Continue | Continue | BP control |
| Allopurinol 100mg | Continue | Continue | No interaction concern acutely |
| Insulin sliding scale | Not prescribed | Add | Glucose control peri-PCI |
| Point | Remember |
|---|---|
| DAPT = Aspirin + P2Y12 inhibitor | Ticagrelor preferred over Clopidogrel in STEMI |
| Metformin + contrast | Always stop before PCI, restart only if eGFR recovers |
| Atorvastatin in CKD | Safe - minimal renal clearance, no dose cap needed |
| Rosuvastatin in CKD eGFR 30-60 | Cap at 20mg |
| STEMI LDL target | <1.4 mmol/L - needs high intensity statin |
| Statin in STEMI | Start/escalate regardless of baseline cholesterol |