Clinical Notes Before Scripts

• Advanced CKD Stage 5 (approaching ESKD) - SCr 1408 µmol/L on admission (baseline 399 in Oct 2025), eGFR severely reduced. Underlying cause: Diabetic Kidney Disease (DKD).
• Hypertensive Emergency - BP 252/116 with acute target-organ damage (APO, worsening renal function, bilateral crepitations). Defined as SBP ≥180/DBP ≥120 WITH evidence of acute end-organ damage.
• Acute Pulmonary Edema (APO) - secondary to fluid overload + hypertensive emergency. Bibasal crepitations, orthopnea, PND, requiring CPAP on arrival.
• Hyperkalemia - K+ 6.1 mmol/L (normal 3.5-5.0).
• Metabolic Acidosis - pH 7.17, HCO3 10.9, pCO2 30 (compensatory respiratory alkalosis).
• Uremia - Urea 33.1 mmol/L, uremic symptoms (vomiting, lethargy).
• Symptomatic Anemia - Hb 8.8 dropping to 6.8 g/dL. Mixed: Renal anemia (EPO deficiency) + IDA (Iron 9.2 µmol/L, TSAT 21%, though ferritin 231 - may be inflammation-driven).
• Hypoalbuminemia - Albumin 26 g/L (adds to edema).

SCRIPT TYPE 1 - CP2 FORMAT (Problem-then-Medicine Flow)

SCRIPT TYPE 1

SECTION A - DEMOGRAPHIC DATA

1. Type 2 Diabetes Mellitus (T2DM) with target organ damage:
   • Diabetic Kidney Disease (DKD)
   • Diabetic Retinopathy
2. Hypertension (HPT)
3. End-Stage Kidney Disease (ESKD) secondary to DKD:
   • Currently applying for zakat-funded Hemodialysis (HD) centre placement
   • Awaiting AVF (Arteriovenous Fistula) appointment in June 2026
   • USCO KUB (6 January 2025): consistent with bilateral renal parenchymal disease

• Previously worked as a cleaner for 5 years
• Blessed with 4 children
• Denies traditional medicine use
• No smoking, alcohol, or drug abuse documented

• BP: 252/116 mmHg (hypertensive emergency)
• HR: 106 bpm (mild tachycardia)
• Temperature: 36.3°C (afebrile)
• SpO2: 100% (on CPAP)
• Lungs: Bilateral crepitations
• CVS: Dual rhythm, no murmur (DRNM)
• Abdomen: Soft, non-tender
• Bilateral pedal edema up to knee level

1. Advanced CKD Stage 5 approaching ESKD - with fluid overload, hyperkalemia, metabolic acidosis, and uremia - secondary to DKD non-compliant to fluid restriction
2. Acute Pulmonary Edema (APO) - secondary to hypertensive emergency
3. Symptomatic anemia - secondary to chronic kidney disease (renal anemia) AND concurrent iron deficiency anemia (IDA)

SECTION B - LABORATORY INVESTIGATIONS

SECTION C - WARD MEDICATION & PHARMACEUTICAL CARE

9 JUNE 2026 - Day 1 of Admission (Emergency Department + Ward)

• Rapidly lowers BP in a titratable, controlled fashion
• Reduces preload - directly alleviating pulmonary congestion
• Reduces myocardial oxygen demand

• For eGFR 10-30 mL/min: IV Co-amoxiclav 1.2 g BD (reduce frequency)
• For eGFR <10 mL/min: IV Co-amoxiclav 1.2 g OD

1. Phosphate binder - for hyperphosphatemia (PO4 2.97 mmol/L; normal 0.8-1.45 mmol/L)
2. Calcium supplementation - for hypocalcemia (Ca2+ 1.86 mmol/L; normal 2.1-2.6 mmol/L)

10 JUNE 2026 - Day 2

• Patient weaned from CPAP to NPO2 (Nasal Prong O2)
• SOB improving
• BP improved from 252/116 → 145/83 mmHg (post-HD and GTN)
• HD completed (2 hours, UF 2.0 L + blood transfusion - 10% PC transfusion)
• K+ improved from 6.1 → 4.6 mmol/L
• Hb dropped from 8.8 → 6.8 g/dL (dilutional + ongoing bone marrow suppression)

• IV GTN: planned to wean off by evening
• IV Frusemide 80 mg TDS → Oralised to Tab Frusemide 80 mg TDS (first dose at 6 PM, 10/6)
  • Note: IV doses at 6 AM were given; 12 PM and 6 PM doses were not given IV as oralisation had begun
• Tab Zincofer 1/1 OD given
• Tab CaCO3 500 mg BD given (7 AM and 5 AM noted)
• Oral Kalimate 15 g TDS continued (given at 8 AM, 4 PM, 10 PM)
• DXT QID monitoring continued
• Dietitian reviewed: Low sodium, low potassium, low phosphate diet recommended

11 JUNE 2026 - Day 3

• Patient on Room Air (RA), SpO2 97%
• BP 130/62 mmHg - significantly improved
• K+ 4.8 mmol/L (normalised)
• Hb 6.6 g/dL (still low - persistent anemia)
• I/O: near balance (+50 mL) - improved fluid balance
• 4-hour HD planned today (QB 250, QD 500, heparin normal)

• Off IV GTN - discontinued (BP controlled)
• Oral Kalimate stopped - K+ normalized after HD and Kalimate treatment
• CBD removed - off continuous bladder drainage
• Tab Frusemide 80 mg TDS continued (given 7 AM, 1 PM, 6 PM)
• Tab Zincofer 1/1 OD continued
• Tab CaCO3 500 mg BD (7 AM only on 11/6) → Plan changed to CaCO3 1 g TDS (not given yet)
• Tab Rosuvastatin 20 mg ON resumed - patient's own medication
• Plan to transfuse 1 unit packed cells (1Q) during HD - this was requested but not granted due to blood group A+ stock shortage.

SECTION D - PHARMACEUTICAL CARE PLAN

• Issue: Patient has ESKD (eGFR estimated <10 mL/min based on SCr 1408 µmol/L). IV Co-amoxiclav 1.2 g TDS is an overdose in severe renal impairment.
• Recommendation: Reduce frequency to OD or at most BD. Or switch to appropriate antibiotic with confirmed renal dosing. Monitor for signs of antibiotic toxicity.
• Rationale: Amoxicillin is renally excreted (60-80% unchanged in urine). Accumulation in ESKD can cause neurotoxicity (seizures, myoclonus), especially at high doses.

• Issue: Morphine's active metabolite M6G accumulates in renal failure, causing respiratory depression and prolonged sedation.
• Recommendation: If morphine was used, monitor closely for respiratory depression. Consider opioid alternatives (e.g., hydromorphone with dose reduction, or non-opioid alternatives).

• Issue: Basal insulin was withheld during admission. As patient stabilises, basal insulin reinstatement should be evaluated to maintain glycemic control.
• Recommendation: Reassess basal insulin need on 15/6 and beyond, with DXT monitoring.

• Issue: CaCO3 as phosphate binder is most effective when taken with or immediately before meals.
• Recommendation: Ensure patient and nursing staff are educated that CaCO3 must be taken with food for phosphate-binding effect. If taken on an empty stomach, it acts only as calcium supplement but not phosphate binder.

• Vildagliptin 50 mg OD (not the 50 mg BD renal-adjusted dose) was appropriately withheld in ESKD. DPP-4 inhibitors are not appropriate in acute illness and should be reviewed for reinstatement only when patient is stable and eGFR is known.

SCRIPT TYPE 2 - STORYTELLING FORMAT (Diagnosis-first, Medicine follows naturally)

SCRIPT TYPE 2

Who is Puan Losila?

Why did she come in?

What did we find on arrival?

• BP: 252/116 mmHg - this is not just high hypertension; this is a hypertensive emergency because she had clear evidence of acute target-organ damage.
• HR: 106 bpm - tachycardia, likely driven by sympathetic overdrive and hypoxia
• SpO2: 100% - but she needed CPAP to maintain this
• On examination: bilateral lung crepitations (fluid in her lungs), bilateral pedal edema up to knee level, and a congested chest X-ray showing cardiomegaly

What was the diagnosis?

1. Advanced CKD Stage 5 approaching ESKD with a cluster of life-threatening metabolic derangements: fluid overload, hyperkalemia, metabolic acidosis, and uremia - all precipitated by non-compliance to her fluid restriction in the setting of underlying DKD
2. Acute Pulmonary Edema (APO) secondary to Hypertensive Emergency - the extremely elevated BP (252/116) overwhelmed the left ventricle's ability to pump, causing back-pressure into the pulmonary circulation and flooding of the alveoli
3. Symptomatic Anemia - with Hb as low as 6.6 g/dL by Day 3, caused by a combination of renal anemia (reduced erythropoietin production from failing kidneys) and Iron Deficiency Anemia (IDA) (serum iron 9.2 µmol/L, TSAT 21% - both below normal)

Day 1 - 9 June 2026: Stabilising the Crisis

Day 2 - 10 June 2026: Stepping Down

Day 3 - 11 June 2026: Continued Recovery

Looking Ahead - Pending on 15 June 2026

1. Clinical progress and vital signs from 12-14 June
2. Outcome of 11/6 HD - fluid removed, K+ and Hb post-HD
3. Whether blood transfusion was eventually given
4. Status of IJC (Internal Jugular Catheter) insertion - planned for Sunday (14/6) to enable proper vascular access for HD
5. Ongoing medication list and any new prescriptions
6. Progress on HD centre application and AVF planning

Summary of Pharmaceutical Care Issues (PCIs)

Overall Assessment - Any Other PCI?

Quick Clinical Reference: The "7W" Framework for This Case

Key Guideline Sources to Reference in Presentation

• CPG Malaysia Management of Hypertension, 5th Edition (2018) - hypertensive emergency: reduce MAP ≤25% in first hour, IV GTN for APO
• CPG Malaysia Management of Chronic Kidney Disease in Adults, 2nd Edition (2018) - CKD staging, management of complications
• CPG Malaysia Conservative Kidney Management for Advanced CKD, 1st Edition (2025) - conservative management, dialysis planning
• KDIGO CKD 2024 Clinical Practice Guideline - CKD classification, anemia, MBD management
• KDIGO Anemia in CKD - Hb targets, iron indices (TSAT <30%, ferritin <500 = trial of iron), ESA thresholds
• KDIGO CKD-MBD - phosphate binders, calcium targets in CKD

Note for 15 June: When you return, look specifically for: new medication additions, whether metformin was ever listed (it should be stopped in ESKD - though not seen here), whether EPO/Darbepoetin was started (anemia of CKD - Hb <10 is the threshold per KDIGO), outcome of IJC insertion, and whether the CaCO3 dose was escalated to 1g TDS as planned.

Complete Script: Zincofer (Oral Iron) PCI + ESA Discussion

BACKGROUND KNOWLEDGE: Understanding the Anemia in This Patient

• Serum Iron: 9.2 µmol/L (low; normal 13-27)
• Transferrin: 1.5 g/L (low; normal 2.0-3.6) - reduced synthesis, partly due to hypoalbuminaemia
• TSAT: 21% (low-normal; normal 15-50%)
• Ferritin: 231 ng/mL (within normal; but ferritin is an acute phase reactant - it may be falsely elevated due to inflammation, masking true iron deficiency)
• Hb: 8.8 → 6.6 g/dL (progressively falling)

• Absolute iron deficiency: True depletion of body iron stores (ferritin <100 ng/mL)
• Functional iron deficiency: Iron stores may be adequate but iron cannot be mobilised fast enough to meet the demands of the bone marrow - often due to hepcidin excess. Hepcidin is a hepatic peptide that blocks ferroportin (the iron export channel on intestinal cells and macrophages), preventing iron absorption from the gut and iron release from stores. In CKD and chronic inflammation, hepcidin levels are chronically elevated. This explains why oral iron has poor efficacy in CKD - even if iron is ingested, hepcidin blocks its absorption.

SCRIPT SECTION: Tab Zincofer - Full CP2 Presentation

FOR SCRIPT TYPE 1 (Medicine-First Format):

1. Chronic renal anemia (EPO deficiency from ESKD)
2. Concurrent absolute/functional iron deficiency

PCI IDENTIFIED: Route of Iron Administration - Oral (Tab Zincofer) vs Intravenous Iron

"In people with anemia and CKD G5HD who are initiating iron therapy, we suggest using intravenous (i.v.) iron rather than oral iron."

"We recommend that most people on haemodialysis will require IV iron."

"Parenteral iron is the treatment of choice for absolute and functional iron deficiency in HD patients because oral iron has low efficacy in CKD. Parenteral iron can easily be administered during dialysis in patients receiving HD."

1. Hepcidin elevation: In CKD and chronic inflammation, hepcidin levels are chronically elevated. Hepcidin binds ferroportin on intestinal enterocytes and macrophages, blocking iron absorption from the gut. No matter how much oral iron is given, hepcidin prevents it from reaching the bloodstream. This renders oral iron largely ineffective in CKD patients.
2. Additional iron losses in HD patients: Hemodialysis patients have additional iron losses not seen in non-HD patients - from blood retained in dialysis tubing and filters (approximately 1-2 g/year), from frequent blood sampling, and from gastrointestinal microbleeds. These losses outstrip the gut's limited capacity to absorb oral iron.
3. GI side effects: Oral iron causes dose-dependent gastrointestinal side effects (nausea, constipation, abdominal discomfort), reducing adherence - particularly in CKD patients who already have GI symptoms from uremia, such as Puan Losila who presented with vomiting and loose stools.
4. IV iron bypasses the gut entirely: IV iron - such as iron sucrose (Venofer), ferric carboxymaltose (Ferinject), or ferric gluconate - is administered directly into the bloodstream during HD sessions, where it is taken up by the reticuloendothelial system and rapidly made available for erythropoiesis. The PIVOTAL trial (2019) demonstrated that proactive high-dose IV iron sucrose (400 mg monthly) was superior to reactive low-dose IV iron in reducing cardiovascular events, mortality, ESA requirements, and RBC transfusions in CKD G5HD patients.

• CKD G5, approaching ESKD (SCr 1408, on HD during this admission)
• Ferritin 231 ng/mL (≤500) and TSAT 21% (≤30%) - KDIGO 2026 Recommendation 2.1 criteria for initiating iron in CKD G5HD are MET
• Already on HD (2 sessions during this admission; long-term HD is the RRT plan)
• Has symptomatic anemia (Hb dropping from 8.8 → 6.6 g/dL)
• Has GI symptoms (vomiting, loose stool) that would worsen with oral iron

1. Switch from Tab Zincofer (oral iron) to IV iron - specifically, IV iron sucrose (iron sucrose 100-200 mg per dialysis session, administered during the HD session) is the preferred choice. This eliminates the GI burden, bypasses the hepcidin block, and is directly available during dialysis.
2. Per KDIGO 2026 Practice Point 2.1: "In people with CKD G5HD in whom iron therapy is being initiated, administer IV iron using a proactive approach to maintain stable iron status."
3. The goal iron parameters to target: TSAT 20-30% and ferritin 200-500 ng/mL during maintenance iron therapy.
4. Withhold iron if ferritin >700 ng/mL or TSAT ≥40% (per KDIGO 2026 Practice Point 2.2).

SECOND PCI: ESA (Erythropoiesis-Stimulating Agent) Not Yet Initiated - Is This Appropriate?

• 9/6 (2 AM): Hb 8.8 g/dL
• 9/6 (11:45 PM): Hb 6.8 g/dL
• 11/6: Hb 6.6 g/dL

"In people with anemia and CKD G5D receiving HD or peritoneal dialysis, we suggest initiation of ESA therapy when the Hb concentration is ≤9.0-10.0 g/dl."

• Starting ESA in an iron-deficient patient causes a "functional iron deficiency" - the bone marrow is stimulated to produce RBCs faster than iron can be supplied, leading to ESA hyporesponsiveness.
• KDIGO guidelines explicitly state: iron stores should be replete (or at least iron therapy initiated) before or concurrent with ESA initiation.

• The patient's anemia may have multiple reversible contributing factors (acute blood loss during HD, haemodilution, GI losses)
• Active fluid overload and electrolyte disturbances must be stabilised first
• In acute severe anemia with Hb <7 g/dL, blood transfusion is the immediate intervention (not ESA, as ESA takes 2-4 weeks to show effect)

1. ESA initiation is indicated for Puan Losila given her Hb ≤9.0 g/dL on HD (per KDIGO 2026 Rec 3.2.1).
2. Ensure IV iron is established first (switch from oral Zincofer to IV iron sucrose during HD).
3. Once iron is being given and acute illness is stabilised, initiate ESA therapy:
   • Epoetin alfa (EPO) SC injection, 3x per week or per dialysis session, starting dose 50-100 IU/kg
   • OR Darbepoetin alfa (longer half-life, once weekly or once fortnightly)
4. Target Hb: 10-11.5 g/dL (per KDIGO 2026 - do not exceed 11.5 g/dL to avoid cardiovascular events and thrombosis)
5. Monitor Hb every 2-4 weeks after ESA initiation and adjust dose to avoid a rapid rise of >1 g/dL per 2-4 weeks
6. ESA should NOT be used to raise Hb above 13 g/dL (per KDIGO 2026 Recommendation 3.6 - strong 1A)

FOR SCRIPT TYPE 2 (Storytelling Format):

1. Switch oral Zincofer to IV iron sucrose (to be given during HD sessions)
2. Once IV iron is established and the patient is clinically stable, initiate ESA - either Epoetin alfa (SC, 3x per week) or Darbepoetin alfa (SC, once weekly). The target Hb should be 10.0-11.5 g/dL - do not exceed 11.5 g/dL, as higher Hb targets with ESA are associated with increased risk of stroke, cardiovascular events, and thrombosis (KDIGO 2026 Recommendation 3.6 - Grade 1A).
3. An important point for Puan Losila specifically: she is 48 years old with ESKD, and future kidney transplantation is a realistic consideration in her care pathway. Repeated blood transfusions form HLA antibodies that reduce transplant compatibility. This is another strong reason to establish ESA + IV iron as the sustainable management strategy rather than relying on transfusions.

Summary Table: Zincofer PCI + ESA Discussion

Tip for presentation: When your preceptor asks "Why not just give oral iron?" - lead with the hepcidin mechanism first. It shows you understand the pathophysiology, not just the guideline statement. Then back it up with KDIGO 2026 Recommendation 2.2 and the PIVOTAL trial evidence. That combination of mechanism + evidence + guideline is what impresses a strict preceptor.

UPDATED SCRIPTS: Days 4-7 (12 June - 15 June 2026)

FIRST: Answer to Your Clinical Question About BP on Day 6 (14 June)

Is BP 143/75 mmHg on 14 June "Normal"? Or Resistant/Refractory Hypertension? And Is Prazosin Needed?

"Reduce BP by no more than 25% within the first hour; then, if stable, to 160/100 mmHg within the next 2 to 6 hours; and then cautiously to normal during the following 24 to 48 hours in all other situations."

"BP lowering until symptom resolution: <25% within 1 hour, then ≤160/100 mmHg over 2 to 6 hours."

• Standard BP target for most patients: <140/90 mmHg
• Target for patients with diabetes mellitus: <140/80 mmHg
• Target for patients with renal impairment / CKD: <130/80 mmHg

1. She is still in hospital
2. She has been through a severe hypertensive emergency just 6 days ago
3. Her BP trend is downward and stabilising
4. Volume status is improving (I/O improving, HD ongoing)

"Resistant hypertension is defined as uncontrolled hypertension (>140/90 mmHg) with good medication adherence while on three or four anti-hypertensive agents (including a diuretic) in adequate doses."

1. Medication non-adherence - she was previously non-compliant to fluid restriction; this may extend to medications
2. Volume overload - she is still fluid-overloaded (post-HD, I/O still not fully balanced); volume is the single biggest driver of hypertension in CKD/ESKD
3. White coat effect / office hypertension
4. Secondary causes

1. T. Metoprolol 100 mg BD (beta-blocker)
2. T. Felodipine 10 mg BD (CCB - but wait: the new data states Felodipine 40 mg BD - this needs clarification, as the standard maximum dose of felodipine is 20 mg/day; 40 mg BD would be 80 mg/day which is well above the maximum dose of 20 mg/day - this is a PCI)
3. T. Frusemide 80 mg TDS (loop diuretic)

1. Volume-driven hypertension not yet fully treated: The primary cause of persistent hypertension in ESKD is volume overload. Her HD program is just starting (IJC inserted 14/6). As regular HD removes excess fluid and she approaches her dry weight, BP should fall further. Adding more antihypertensives before optimising dialysis is premature.
2. BP is trending down: From 195/91 on Day 4 → 149/80 on Day 5 → 143/75 on Day 6. The current regimen is working.
3. Prazosin risks in this patient: Prazosin, an alpha-1 adrenergic blocker, causes venodilation and arteriodilation. It carries a significant risk of first-dose hypotension (orthostatic hypotension), which is particularly dangerous in CKD/HD patients who are already at risk of intradialytic hypotension. Alpha-blockers have not been shown to reduce cardiovascular events in CKD patients (ALLHAT study showed doxazosin was inferior to chlorthalidone for cardiovascular outcomes).
4. Not first-line or second-line for CKD hypertension: Alpha-blockers like prazosin are considered add-on (4th-line) agents for resistant hypertension, not for inadequately controlled hypertension that is still trending towards target.
5. Better 4th-line options exist if needed: Per current evidence in CKD patients, if a 4th agent is needed, spironolactone (an MRA/aldosterone antagonist) has the strongest evidence base for resistant hypertension. However, in ESKD this is limited by hyperkalemia risk. Chlorthalidone is another option per recent evidence in advanced CKD.

1. If after regular HD (twice weekly), adequate volume removal to dry weight, and optimisation of current 3 drugs, BP remains >140/80 mmHg - then a 4th agent is justified.
2. Prazosin is available, cheap, and commonly used in Malaysian public hospitals as add-on therapy.
3. Alpha-blockers do have a role in resistant hypertension in CKD - they cause vasodilation and reduce sympathetic outflow, which is chronically elevated in ESKD.
4. The KIV prazosin notation in the notes is appropriate clinical practice - "Keep in View" if BP persistently high, not a confirmed decision to start.

Prazosin is NOT needed at this point. The BP at 143/75 mmHg is marginally above target and still trending down. The primary therapeutic priority is optimising dialysis (adequate volume removal to dry weight) and ensuring medication adherence. If BP remains persistently above 140/80 mmHg after several weeks of regular HD and full dose optimisation, then adding a 4th agent (with prazosin as one option, though not the most evidence-based choice) would be reasonable. The KIV notation in the notes is clinically appropriate.

FELODIPINE 40 MG BD - CRITICAL PCI

• Standard dose: 5-10 mg OD (some sources allow up to 20 mg OD)
• Maximum recommended dose: 20 mg/day

1. Documentation error - the patient's home medication was Felodipine 10 mg BD (as per the earlier records), and "40 mg BD" is a transcription error in your notes
2. Tablet strength confusion - felodipine is available as 2.5 mg, 5 mg, 10 mg tablets; there is no 40 mg felodipine tablet commercially available in Malaysia
3. It is possible this refers to a different drug written incorrectly

UPDATED SCRIPT TYPE 1 (Days 4-7: Medicine-First Format)

12 JUNE 2026 - Day 4

• BP: 195/91 mmHg - still elevated but trending down from 252/116 on admission
• I/O: -350 mL (negative balance - diuresis working, HD effect)
• Plan: Keep over weekend; IJC insertion and HD planned for Sunday (14/6)

• T. Metoprolol 100 mg BD (8 AM, 4 PM)
• T. Felodipine 10 mg BD (8 AM, 4 PM) (please verify - refer PCI above regarding the 40 mg figure)
• T. Frusemide 80 mg TDS
• T. Zincofer 1/1 OD
• T. CaCO3 (ongoing)
• T. Rosuvastatin 20 mg ON

13 JUNE 2026 - Day 5

• BP: 149/80 mmHg - improved further
• I/O: +200 mL (slightly positive balance)
• S/C Actrapid given at 5 PM (DXT >12 mmol/L threshold)
• Plan: Aim for IJC insertion Sunday; HD Sunday; continue medications

14 JUNE 2026 - Day 6

• BP: 143/75 mmHg - near-target
• Minimal bilateral pedal edema (significant improvement from knee-level edema on Day 1)
• Able to lie flat - resolved APO (previously could not lie flat due to orthopnea)
• Last HD was on Thursday (11/6)
• IJC inserted today at 4 PM (X-ray confirmed IJC in situ, no hematoma, no blood clot)
• Plan for HD post-IJC insertion
• ACC lodging arranged for ongoing twice-weekly HD while awaiting zakat approval

1. Advanced CKD approaching ESKD - RRT: HD; AVF appointment 13 July 2026 (updated from 3 July)
2. Resolved APO secondary to Hypertensive Emergency - see BP analysis above
3. DM - controlled (DXT 6.7-5.9 mmol/L on ward days; S/C Actrapid PRN used appropriately)

• T. Metoprolol 100 mg BD (8 AM, 4 PM) - continued
• T. Felodipine 10 mg BD (8 AM, 4 PM) - continued (PCI: verify dose - do NOT accept 40 mg BD)
• T. Frusemide 80 mg TDS - continued
• T. Zincofer 1/1 OD - continued
• T. CaCO3 1 g TDS (8 AM, 11:30 AM, 5:30 PM) - from 11/6 5:30 PM, taken with meals
• T. Rosuvastatin 20 mg ON - from 11/6
• S/C Actrapid given at 5 PM PRN

S/C ACTRAPID (Regular Insulin) - Full Timeline

• 9/6 at 10 PM
• 11/6 at 5 PM
• 13/6 at 5 PM
• 14/6 at 5 PM
• 15/6 at 6 AM

15 JUNE 2026 - Day 7 (Today)

• Post-HD clinical status (HD done after IJC insertion on 14/6)
• Current Hb, electrolytes, renal profile post-HD
• BP on today's ward round
• Whether blood transfusion was given (1Q PC - previously not granted due to stock shortage)
• Progress on ACC lodging for twice-weekly HD
• Discharge planning timeline
• Reinstatement of Insugen N and Vildagliptin

UPDATED SCRIPT TYPE 2 (Days 4-7: Storytelling Format)

COMPLETE MEDICATION TABLE - DAYS 1 TO 7

COMPLETE PCI SUMMARY TABLE (All Days)

Key message for your preceptor: The most impactful PCIs to present are #1 (Augmentin dose adjustment), #3 (oral vs IV iron), and #4 (ESA not initiated). These are the ones with the clearest evidence base and direct patient safety implications. Present #6 (felodipine dose) as a documentation query - it shows attention to detail. PCIs #7 and #8 are forward-looking and show clinical foresight about discharge planning.

IJC vs AVF - Why Both Are Needed

The IJC (Internal Jugular Catheter) - Temporary Bridge

The AVF (Arteriovenous Fistula) - Permanent, Lifelong Access

The Timeline for Puan Losila - Why Both Are Needed Simultaneously

ESKD diagnosed / decompensation occurs
         ↓
Insert IJC immediately → Start HD now (bridge access)
         ↓
Create AVF surgically (appointment 13 July 2026 for Puan Losila)
         ↓
Wait 6-8 weeks for AVF to mature (arterialization of the vein)
         ↓
Vascular access team confirms AVF is ready (sufficient diameter and flow)
         ↓
Switch dialysis to AVF (needle the fistula for HD)
         ↓
Remove IJC (no longer needed)

• Now: HD via IJC (temporary) at ACC lodging twice weekly
• 13 July 2026: AVF creation surgery
• ~September 2026 (estimate): AVF maturation, confirmation, first cannulation
• After AVF confirmed working: IJC removed

One More Layer - Why AVF Creation Needs Planning (Not Just Insertion)

1. Vein mapping - ultrasound to assess which veins are suitable (adequate diameter, no pre-existing damage)
2. Artery assessment - ensure adequate arterial inflow
3. Dominant hand consideration - AVF is usually created in the non-dominant arm to preserve function
4. Preserving veins - patients with upcoming AVF should not have blood taken or IVs placed in the forearm/antecubital fossa of the planned AVF arm, as even a single cannulation can damage veins

Summary in One Sentence for Your Presentation

"The IJC is a temporary bridge access to enable urgent HD now, while the AVF - which takes 6-8 weeks to mature after surgical creation - is being planned as the permanent, superior, long-term dialysis access. The goal is to transition from IJC to AVF as quickly as possible to reduce infection, thrombosis, and vascular complications associated with long-term catheter use."

ISSUE 1: Calcium 12.9 mmol/L and Phosphate 22.6 mmol/L while on CaCO3 1g TDS

First - Are These Values Real?

• Calcium 12.9 mmol/L - the normal range is 2.1-2.6 mmol/L. A value of 12.9 mmol/L would be extreme, life-threatening hypercalcemia (>3.5 mmol/L is already a medical emergency causing coma, cardiac arrest). If this is correct, the patient would be severely symptomatic - altered consciousness, vomiting, bradycardia.
• Phosphate 22.6 mmol/L - normal is 0.8-1.45 mmol/L. A value of 22.6 mmol/L is impossibly high for a living patient - even in the most severe ESKD, phosphate rarely exceeds 4-5 mmol/L.

1. mg/dL reported, not mmol/L - In some labs and in the US system, calcium is reported in mg/dL (normal 8.5-10.5 mg/dL) and phosphate in mg/dL (normal 2.5-4.5 mg/dL). If so, Ca 12.9 mg/dL = mild-moderate hypercalcemia, and Phosphate 2.2 mg/dL = hypophosphatemia (low). The picture changes completely.
2. Transcription/documentation error on the lab printout
3. Haemolysed sample causing spurious results

BUT - If Calcium IS Truly Elevated (Even in mg/dL, e.g. 12.9 mg/dL = 3.22 mmol/L):

The PCI: CaCO3 1 g TDS Continued Despite Hypercalcemia

"In adult patients with CKD G3a-G5D, we suggest avoiding hypercalcemia."

"In patients with CKD G3a-G5D and hyperphosphatemia, we recommend restricting the dose of calcium-based phosphate binders and/or calcitriol in the presence of persistent or recurrent hypercalcemia."

"In adult patients with CKD G3a-G5D receiving phosphate-lowering treatment, we suggest restricting the dose of calcium-based phosphate binders."

1. Phosphate binder - taken with meals, binds dietary phosphate in the gut
2. Calcium supplement - provides elemental calcium, raising serum calcium

• Vascular calcification (calcium deposits in blood vessel walls) - raising CV mortality
• Soft tissue calcification
• Adynamic bone disease
• Cardiac arrhythmias
• Worsening hypertension

1. Withhold Calcium Carbonate immediately in the presence of hypercalcemia - per KDIGO 2017 Recommendation 4.1.5 (1B)
2. Switch to a non-calcium-based phosphate binder - the options available in Malaysia:
   • Sevelamer carbonate (Renvela) - binds phosphate in the gut without adding calcium load; has additional benefits of reducing LDL and uric acid. The INDEPENDENT trial showed significantly lower cardiovascular mortality with sevelamer vs calcium-based binders in HD patients.
   • Lanthanum carbonate (Fosrenol) - another non-calcium binder, effective but more expensive
3. Dietary phosphate restriction should continue (low phosphate diet - already referred to dietitian)
4. HD itself removes phosphate - regular HD sessions will help lower both calcium and phosphate
5. Recheck calcium and phosphate after stopping CaCO3 and after next HD session

"On 14 June, Puan Losila's calcium was found to be elevated at [confirmed value] and phosphate at [confirmed value], while she was on Tab Calcium Carbonate 1 g TDS. I wish to flag this as a Pharmaceutical Care Issue.

Calcium Carbonate serves as both a phosphate binder and a calcium supplement. However, in the presence of hypercalcemia, continuing a calcium-containing phosphate binder is contraindicated - per KDIGO 2017 CKD-MBD Guideline Recommendation 4.1.5, a strong Grade 1B recommendation states that calcium-based phosphate binders should be restricted when hypercalcemia is present. Continued calcium loading in ESKD risks vascular calcification, soft tissue deposition, and cardiac arrhythmias.

My recommendation is to withhold Calcium Carbonate and switch to a non-calcium-based phosphate binder such as Sevelamer Carbonate. Sevelamer does not contribute to calcium load, has additional benefits of reducing LDL and inflammatory markers, and the INDEPENDENT trial demonstrated lower cardiovascular mortality with sevelamer compared to calcium-based binders in HD patients. Dietary phosphate restriction should continue, and HD itself contributes to phosphate removal. Calcium and phosphate levels should be rechecked after the next HD session."

ISSUE 2: I/O Chart - Is It Good or Bad?

• Day 3 (11/6): -350 mL (negative)
• Day 5 (13/6): +200 mL (positive)
• Day 6 (14/6): +300 mL (positive)

Understanding I/O in This Patient

Reading Each Day:

• Oral intake slightly exceeded the 500 mL restriction
• Less urine output that day
• No HD between 11/6 and 14/6 (HD gap over weekend) However, 200 mL positive over one day is small, and the cumulative trend matters more than single-day readings.

• HD had not yet happened when the I/O was recorded (IJC only inserted at 4 PM)
• The 500 mL fluid restriction may not have been fully adhered to
• The gap since last HD (11/6 to 14/6 = 3 days without HD) allows fluid to re-accumulate

Overall Assessment of the I/O Trend:

1. Strict fluid restriction (ROF 500 mL/day) must be reinforced
2. Regular twice-weekly HD is critical - each session removes the fluid that accumulates between sessions
3. Frusemide is continued to maximise residual urine output (she still has some urine output)

"Looking at the I/O chart, we see a negative balance of -350 mL on 11/6 - this is favourable, reflecting the combined effect of oral frusemide TDS and HD. However, by 13/6 and 14/6, the balance turned positive at +200 and +300 mL respectively. This is expected in ESKD patients over a 3-day HD gap - fluid re-accumulates between sessions because the kidneys can no longer excrete sodium and water. Notably, HD was performed on 14/6 post-IJC insertion, and the ultrafiltration volume from HD would not be captured in the ward I/O chart - so the true fluid balance on 14/6 is more favourable than the ward chart suggests.

The key clinical takeaway is that regular twice-weekly HD is essential to manage the inter-dialytic fluid accumulation, and strict adherence to the 500 mL/day fluid restriction must be continuously reinforced. The overall admission trend - from severe bilateral edema to knees at Day 1, to minimal pedal edema and ability to lie flat by Day 6 - confirms that the fluid management strategy has been effective."

Summary for Quick Reference