Ventilator setting in copd

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"mechanical ventilation" AND "COPD" AND settings

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Ventilator Settings in COPD

COPD patients have airflow obstruction, air trapping, and intrinsic PEEP (iPEEP). All ventilator decisions revolve around one central goal: maximize expiratory time to prevent dynamic hyperinflation.

1. Non-Invasive Ventilation (NIV) - First Choice in Acute Exacerbation

NIV (BiPAP) is the preferred initial ventilatory support in AECOP. It avoids intubation in the majority of patients.

Parameter	Target
Mode	Bilevel PAP (IPAP/EPAP)
IPAP (Inspiratory)	Start 10-12 cmH2O, titrate up to reduce PCO2
EPAP (Expiratory)	4-5 cmH2O (to counteract iPEEP)
Backup RR	10-14/min
FiO2	Titrate to SpO2 88-92%
Goal	PCO2 reduction within 1-2 hours; pH improvement

Improvements in pH, PCO2, and level of consciousness within the first 1-2 hours are strong predictors of NIV success.
Home NIV is indicated in chronic stable hypercapnic COPD patients with PaCO2 > 52 mmHg. After an acute episode, use only if hypercapnia (PCO2 > 48 mmHg) persists at 2-4 weeks post-discharge. Fixed pressure mode is preferred over auto-titrating modes.

2. Invasive Mechanical Ventilation - Indications

Invasive ventilation is needed when NIV fails or is contraindicated:

Severe tachypnea > 35 breaths/min
Respiratory arrest or apnea
Severe/worsening acidosis + hypercapnia
Hemodynamic instability (shock)
Somnolence / altered mental status
Life-threatening hypoxemia

3. Recommended Invasive Ventilator Settings

Mode

Volume-controlled Assist-Control (VC-AC) is the most common initial choice - it gives control over tidal volume, which is critical to prevent dynamic hyperinflation.
Pressure-control can also be used but requires monitoring tidal volumes closely since they vary with changing resistance and compliance.

Key Parameters

Parameter	Recommended Setting	Rationale
Tidal Volume (VT)	5-8 mL/kg predicted (IBW)	Avoid hyperinflation. 5-7 mL/kg (Murray & Nadel) or ≤8 mL/kg (Rosen's)
Respiratory Rate (RR)	10-14/min	Low rate lengthens expiratory time; every decrease in rate has a large effect on expiratory time
I:E Ratio	1:3 to 1:4	Prolonged expiration allows air trapping to resolve
Inspiratory Flow Rate	60-80 L/min (high flow)	Shorter inspiration = longer expiration
PEEP (External)	5 cmH2O (initial)	Counterbalances iPEEP; safe for all COPD patients initially
FiO2	Titrate to SpO2 88-92%	Avoid hyperoxygenation; prevents loss of hypoxic drive and worsens V/Q
Plateau Pressure	< 30 cmH2O	Monitor to exclude additional lung injury

4. The iPEEP Problem - Central to COPD Ventilation

Intrinsic (auto) PEEP builds up because patients cannot fully exhale before the next breath. This causes:

Air trapping and dynamic hyperinflation
Reduced venous return - can mimic cardiogenic shock
Patient-ventilator dyssynchrony (patient can't reach trigger threshold)
Hypotension

How to detect iPEEP: End-expiratory hold maneuver on ventilator. Total PEEP minus set PEEP = iPEEP.

How to reduce iPEEP:

Decrease RR - most effective
Decrease tidal volume
Shorten inspiratory time (increase flow rate)
Bronchodilators + corticosteroids (reduce airway resistance)
Set external PEEP at 50-80% of iPEEP (to reduce inspiratory threshold load and improve triggering)

If hemodynamic collapse occurs and iPEEP is suspected, temporarily disconnect from ventilator - rapid resolution of hypotension confirms iPEEP as the cause (not cardiogenic shock).

5. Permissive Hypercapnia

COPD patients often have chronic CO2 retention. Do not chase normal PaCO2. Attempting to normalize PaCO2 forces higher RR/VT - this worsens dynamic hyperinflation.

Accept PCO2 elevation as long as pH > 7.2
Tolerate respiratory acidosis - it will improve with bronchodilators and time
If pH < 7.2: cautiously increase RR first (watch for iPEEP), then consider increasing VT

6. Pressure-Support Ventilation in COPD

PSV is useful for weaning but has a specific problem in COPD: because of the prolonged time constant (high resistance), flow takes longer to fall to the cycling threshold, so mechanical inflation persists into neural expiration. This causes:

Expiratory muscle activation fighting the ventilator
Patient-ventilator dyssynchrony ("fighting the ventilator")

Solution: Reduce the cycling-off threshold (increase the flow termination % from 25% to a higher value on the ventilator) to cycle the breath off sooner.

7. Troubleshooting Summary

Problem	Action
High PaCO2, pH > 7.2	Tolerate; treat with bronchodilators
High PaCO2, pH < 7.2, no iPEEP	Cautiously increase RR
High PaCO2, pH < 7.2, iPEEP present	Increase VT, keep rate low
High peak pressure (normal plateau)	Increased airway resistance - check tube, mucus plug; continue bronchodilators
High peak AND plateau pressure	Decreased compliance - consider pneumothorax, worsening
Hypotension on ventilator	Suspect iPEEP - disconnect briefly to confirm; reduce rate/VT

Sources:

Murray & Nadel's Textbook of Respiratory Medicine, 2-Vol (section: Invasive Mechanical Ventilation in COPD)
Rosen's Emergency Medicine, 10e (section: Acute Exacerbation of COPD, Invasive Ventilation)
Fishman's Pulmonary Diseases and Disorders (section: Pressure-Support Ventilation / Triggering)

Remifentanyl

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Remifentanil

Overview

Remifentanil is the first and only ultra-short-acting opioid available for clinical use. It is a piperidine derivative structurally related to fentanyl, but uniquely different because of its ester linkages - these make it susceptible to hydrolysis by blood and tissue non-specific esterases, giving it a rapid and predictable offset completely independent of hepatic or renal function.

Pharmacokinetics

Property	Detail
Class	mu-opioid receptor (MOR) agonist
Onset	1-1.5 min after IV bolus
Peak respiratory depression	~5 min after bolus
t½	8-20 min; context-insensitive half-life ~3-4 min
Metabolism	Plasma and tissue non-specific esterases (de-esterification)
NOT a substrate for	Pseudocholinesterase - unaffected by pseudocholinesterase deficiency
Main metabolite	GI90291 (carboxylic acid) - only 0.001 to 0.003 times as potent as parent
Metabolite excretion	Renal
Protein binding	~70% (mostly to alpha-1-acid glycoprotein)
pKa	7.07 (weak base)
PK model	Three-compartment
Clearance	Several times greater than normal hepatic blood flow - confirms widespread extrahepatic metabolism
Lung metabolism	Not significantly metabolized in lungs
Recovery of respiratory function	3-5 min after 3-5 hour infusion
Full effect offset	Within 15 min

Key point: Because metabolism is by non-organ esterases, hepatic or renal failure does not significantly alter pharmacokinetics. This makes it especially useful in patients with liver/kidney failure (including infants with hepatic or renal failure).

Potency

100-200 times more potent than morphine
Large inter-patient variability: the CP50 for no response to laryngoscopy/intubation ranges 50-fold (1.5 to 79 ng/mL)
Gender differences exist: CP50 ~4.1 ng/mL in men vs 7.5 ng/mL in women (partly attributable to differences in surgical nociception)

Pharmacodynamics / Clinical Effects

CNS / Analgesia

Potent analgesia with rapid onset and offset
Reduces MAC of volatile anesthetics significantly (e.g., remifentanil at 3 ng/mL + sevoflurane: MAC reduced to ~0.36% from ~3.96%)
Reduces propofol requirements >60% (propofol CP50 for laryngoscopy drops from 7 to 3 mcg/mL with remifentanil 2 ng/mL)
At sedative doses (0.05-0.15 mcg/kg/min) can increase CBF in prefrontal, inferior parietal, and supplementary motor cortices
At moderate anesthetic doses in craniotomy: ICP unchanged, CBF comparable to balanced anesthesia

Respiratory

Causes dose-dependent respiratory depression
No delay between plasma concentration and ventilatory effect (unlike slower opioids)
Safe to use at low infusion rates (< 0.1-0.2 mcg/kg/min) in spontaneously breathing patients with adequate monitoring

Cardiovascular

Generally stable; bolus doses can cause transient hypotension (drop in MAP), which can reflexively increase ICP - so bolus infusion should be used cautiously in head-injured patients

Dosing (Intraoperative)

Indication	Dose
Balanced anesthesia infusion	0.1-1.0 mcg/kg/min
Spontaneous breathing / sedation	< 0.1-0.2 mcg/kg/min
Return of spontaneous ventilation	~0.1 ± 0.05 mcg/kg/min
TIVA with propofol	Target 3-8 ng/mL (titrate to response)
Optimal TIVA concentration for fastest awakening	Remifentanil ~4.8 ng/mL + propofol ~2.5 mcg/mL (wake-up ~7 min)

Because of its very short duration, remifentanil must be given by continuous infusion - bolus alone is not useful for maintenance.

Special Considerations

1. Post-Operative Pain - Critical Concern

Remifentanil's rapid offset means no residual analgesia after infusion stops. Patients frequently experience significant post-operative pain ("fast-track" anesthesia problem):

Post-op pain scores higher, morphine requirements increased after remifentanil-based anesthesia
Strategies: Start morphine 30-45 min before end of surgery, OR give single fentanyl bolus 50 mcg or ketamine 0.125 mg/kg at end of surgery

2. Opioid-Induced Hyperalgesia (OIH)

High doses of remifentanil can paradoxically lower the pain threshold after discontinuation - a phenomenon known as OIH. This contributes to the post-operative pain problem. Ketamine (0.15 mg/kg + 2 mcg/kg/min infusion) can reduce intraoperative remifentanil requirements and post-op morphine consumption.

3. NOT for Intrathecal / Epidural Use

The formulation contains glycine (used to solubilize the free base). Glycine is an inhibitory neurotransmitter that causes reversible motor weakness when injected intrathecally - therefore remifentanil is contraindicated for spinal or epidural administration.

4. Hemorrhagic Shock

Altered pharmacokinetics in hemorrhagic shock - less remifentanil required to maintain target plasma concentration. However, because of rapid metabolism, changes in context-sensitive half-life are less clinically relevant.

5. Pediatrics / Organ Failure

Since elimination is independent of liver and kidney, it is useful in neonates and infants with hepatic or renal failure.

Clinical Indications

Intraoperative analgesia/anesthesia supplement (TIVA with propofol, balanced anesthesia)
Short painful procedures requiring intense analgesia
Blunting of hemodynamic stress responses (laryngoscopy, intubation, surgical stimulus)
PCA analgesia (with adequate monitoring)
ICU sedation/analgesia
Obstetric labor analgesia
Diagnostic procedures

Comparison with Other Fentanyl Congeners

Drug	Onset	Duration	Context-sensitive t½
Fentanyl	Fast	Intermediate	Increases with infusion duration
Alfentanil	Fastest	Short	~1 hour
Sufentanil	Fast	Long	Increases with infusion
Remifentanil	Fast	Ultra-short	~3-4 min - does NOT accumulate

Remifentanil is unique in that its context-sensitive half-life remains ~3-4 minutes regardless of how long the infusion runs - a property no other opioid shares.

Sources:

Miller's Anesthesia, 10e (Ch. 22 - Opioids; Ch. 3 - Cerebrovascular effects)
Barash, Cullen & Stoelting's Clinical Anesthesia, 9e (Ch. 20)
Goodman & Gilman's Pharmacological Basis of Therapeutics (Ch. 7)

Inj Ferrous carboxy maltose

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Injection Ferric Carboxymaltose (FCM)

What It Is

Ferric carboxymaltose (brand name: Ferinject/Injectafer) is a third-generation IV iron preparation consisting of a ferric hydroxide core surrounded by a carboxymaltose carbohydrate shell. Unlike older preparations (especially high-molecular-weight iron dextran), it does not carry significant anaphylaxis risk and does not require a test dose. It allows delivery of large replacement iron doses in a single, short infusion.

Structure & Mechanism

Iron content: 50 mg/mL of elemental iron
The nanoparticle structure is taken up by macrophages of the reticuloendothelial system
Iron is slowly released to transferrin via ferroportin
After IV administration: transient rise in serum iron, ferritin, and transferrin saturation
~80% is distributed to the bone marrow, liver, and spleen
Subsequently corrects hemoglobin and replenishes depleted iron stores

Indications

Iron deficiency anemia - when oral iron is ineffective or not tolerated
Oral iron malabsorption - inflammatory bowel disease, bariatric surgery, short-bowel syndrome, celiac disease, H. pylori infection
Ongoing blood loss too great for oral iron to overcome
Pregnancy (2nd and 3rd trimester) - shown superior to oral iron
Heart failure with iron deficiency - with or without anemia (ESC Class IIa recommendation for HFrEF)
CKD (non-dialysis and dialysis patients)
Perioperative anemia management
Pre-dialysis and hemodialysis patients
Patients on erythropoietin therapy
Patients where rapid iron repletion is needed (hemoglobin ≤8 g/dL)

Dosing

Body Weight	Dose	Schedule
≥50 kg	750-1000 mg per dose	2 doses given ≥7 days apart (total 1500 mg)
<50 kg	15 mg/kg per dose	2 doses given ≥7 days apart

Maximum single dose: 1000 mg (administered over 15 minutes)
No test dose required (unlike iron dextran)
Given as slow IV infusion or IV push (per labeling)

Calculating Total Iron Deficit (Ganzoni Formula):

Total iron deficit (mg) = Body weight (kg) × (target Hb - actual Hb) (g/dL) × 2.4 + 500 mg (for stores)

Pharmacokinetics

Parameter	Detail
Onset of effect	Serum iron rises within hours
Hb correction	Begins within 1-2 weeks
Full replenishment	Within 4-8 weeks
Distribution	~80% to marrow, liver, spleen
Clearance	Rapid from circulation (RES uptake)
Hepatic/renal metabolism	Not significantly dependent on either

Advantages Over Other IV Iron Preparations

Feature	FCM	Iron Dextran	Iron Sucrose	Ferric Gluconate
Max single dose	1000 mg	1000 mg	200 mg	250 mg
Infusion time	15 min	1 hour+	Multiple sessions	Multiple sessions
Test dose needed	No	Yes	No	No
Anaphylaxis risk	Low	Higher (HMW)	Very low	Very low
Sessions to full dose	1-2	1	5-10	4-8

Adverse Effects

Common

Headache, dizziness
Nausea, abdominal pain, constipation, diarrhea
Skin rash, flushing
Injection site reactions
Flu-like symptoms 2-5 days after infusion

Important - Hypophosphatemia (FCM-Specific)

This is the most clinically significant adverse effect unique to FCM:

~75% of recipients develop serum phosphorus < 2.0 mg/dL
Mechanism: FCM causes a marked increase in FGF-23 (Fibroblast Growth Factor-23), a phosphaturic hormone secreted by osteocytes
FGF-23 decreases renal tubular phosphate reabsorption - leading to phosphaturia and hypophosphatemia
Usually transient and asymptomatic in most single-infusion patients
Patients receiving multiple high-dose infusions or with pre-existing micronutrient deficiencies are at risk of developing osteomalacia and bone fractures
Monitor phosphate levels in patients receiving repeated courses

Infusion Reactions

Can occur if a small fraction of iron is rapidly released from the nanoparticle core
Manifest as: flushing, hypotension, chest tightness (not IgE-mediated - not true anaphylaxis)
Do NOT require adrenaline; slow infusion rate or pause

Rare

Hypersensitivity reactions (much less common than with high-MW iron dextran)
Transient hypertension

Contraindications

Iron overload (hemochromatosis, hemosiderosis)
Known hypersensitivity to FCM or any component
Non-iron-deficiency anemia (e.g., hemolytic anemia)
First trimester of pregnancy (use 2nd/3rd trimester only)

Use in Heart Failure - Key Trials

FCM is particularly well studied in heart failure:

Trial	Finding
FAIR-HF	Significant improvement in 6-minute walk distance, patient global assessment, and QoL in HFrEF + iron deficiency
EFFECT-HF	Confirmed exercise capacity improvement
CONFIRM-HF	Improved symptoms, QoL, reduced hospitalizations
Meta-analysis (individual patient data)	IV iron reduced recurrent CV hospitalizations + CV mortality (rate ratio 0.59, 95% CI 0.40-0.88)

ESC Guideline recommendation: Screen all HF patients for iron deficiency (Class I). Consider IV FCM in symptomatic HFrEF with iron deficiency (Class IIa). Oral iron has limited benefit in HF (poor absorption and GI side effects).

Monitoring

Serum ferritin and transferrin saturation (TSAT) before and 4-8 weeks after
Hemoglobin response
Serum phosphate - especially with repeated dosing
Avoid if serum ferritin > 800 mcg/L (risk of iron overload)

Sources:

Goodman & Gilman's Pharmacological Basis of Therapeutics (Ch. 45 - IV Iron Formulations)
Goldman-Cecil Medicine, 2-Vol (Ch. 145 - IV Iron Therapy)
Harrison's Principles of Internal Medicine, 22e (Ch. 102 - Iron Deficiency Treatment)
Fuster & Hurst's The Heart, 15e (Ch. 48 - IV Iron in Heart Failure)
Brenner & Rector's The Kidney (Ch. - IV Iron in CKD)

Inj FCM and B12 inj co relation

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"ferric carboxymaltose" AND "vitamin B12" AND deficiency

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PMID: 36438538

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ferric carboxymaltose vitamin B12 injection combined deficiency anemia clinical correlation

Excellent - now I have all the pieces to give a comprehensive, clinically structured answer. The web search revealed a very important finding - FCM actually decreases B12 and folate levels post-infusion, which is a critical clinical correlation.

Inj. Ferric Carboxymaltose (FCM) and Inj. Vitamin B12 - Clinical Correlation

There are five major clinical relationships between these two injections:

1. Co-existing Deficiencies - The Most Common Reason Both Are Given Together

Iron deficiency and Vitamin B12 deficiency frequently coexist in the same patient, especially in:

Condition	Why Both Are Deficient
Malabsorption (celiac disease, short bowel, Crohn's)	Both iron and B12 require intact small bowel for absorption; B12 needs terminal ileum specifically
Bariatric surgery (gastric bypass, sleeve)	Loss of gastric acid/intrinsic factor + reduced absorptive surface = B12 deficiency; reduced iron absorption surface
Strict vegans / vegetarians	Dietary B12 absent; plant-based iron (non-haem) poorly absorbed
Pregnancy	Increased demand for both; common in India and resource-limited settings
Pernicious anemia	Lack of intrinsic factor → B12 malabsorption; often coexists with autoimmune gastritis causing poor iron absorption
Elderly / nutritional deficiency	Poor dietary intake of both
Chronic inflammatory bowel disease	Malabsorption of both micronutrients
Hemodialysis patients	Both losses increased; B12 losses in dialysate + poor dietary intake

Clinical practice in India: In patients with severe anemia, especially in pregnancy, it is common protocol to administer FCM 1000 mg IV + Vitamin B12 500 mcg IM + Folic acid 15 mg together. A hospital-based study from South Gujarat (PMID 36438538) in 100 severely anemic pregnant tribal women using this combination showed:

Hb rise of 2.9 g/dL at 6 weeks
Hb rise of 5.4 g/dL at delivery
63.9% became non-anemic at delivery
No serious adverse effects; no blood transfusion needed

2. FCM Infusion Can REDUCE Serum B12 and Folate Levels - Key Pharmacological Interaction

This is an important and often overlooked finding:

A prospective study measuring labs before and 30 days after FCM infusion found:

Vitamin B12 fell from 422 pg/mL to 402 pg/mL (p < 0.001)
Folate fell from 7.96 ng/mL to 6.54 ng/mL (p < 0.001)

Mechanism: Rapid erythropoietic response triggered by FCM massively increases red cell production. This new erythropoiesis consumes large amounts of B12 and folate (both required for DNA synthesis in developing erythroid precursors). If the patient has borderline B12/folate stores, FCM can precipitate or unmask a functional B12/folate deficiency.

Clinical implication: Always check and replenish B12 and folate before or alongside FCM infusion, particularly in:

Patients with borderline B12/folate levels
Vegetarians/vegans
Pregnancy
Patients with any malabsorption

3. The "Masked MCV" Problem - Diagnostic Pitfall

This is perhaps the most clinically important diagnostic relationship:

Iron deficiency alone → microcytic, hypochromic anemia (low MCV)
B12 deficiency alone → macrocytic, megaloblastic anemia (high MCV)
Combined iron + B12 deficiency → the two effects cancel each other out → normocytic anemia (MCV apparently normal)

Deficiency	MCV	Blood Film
Iron alone	Low (microcytic)	Hypochromic, microcytes
B12 alone	High (macrocytic)	Oval macrocytes, hypersegmented neutrophils
Iron + B12 combined	Normal (deceptively)	Dimorphic film - mixture of microcytes and macrocytes; hypersegmented neutrophils

If you treat such a patient with FCM alone (correcting only iron), the macrocytic component unmasks - the MCV rises and megaloblastic features become apparent. Conversely, treating B12 alone causes the microcytic component to become more prominent. This is why both must be diagnosed and treated simultaneously.

Key teaching point: A "normocytic anemia" in a patient from a high-risk group (vegan, post-bariatric, malnourished, elderly) should prompt checking both iron studies AND serum B12/folate before attributing it to anemia of chronic disease.

4. Sequence and Timing - Practical Co-administration

Can FCM and B12 Inj be given on the same day?

Yes - they are given by different routes and have no pharmacokinetic interaction:

FCM: IV infusion (15 minutes)
B12 (cyanocobalamin/hydroxocobalamin): IM injection

There is no direct drug-drug interaction between them. In clinical practice (especially obstetrics/hematology), they are routinely administered together on the same visit.

Standard Combined Regimen (from clinical evidence):

Drug	Dose	Route	Schedule
FCM	1000 mg	IV infusion over 15 min	Day 1 (and Day 8 if needed for 2nd dose)
Vitamin B12 (cyanocobalamin/hydroxocobalamin)	500-1000 mcg	IM	Day 1, then weekly × 4, then monthly
Folic acid	5-15 mg	IM or oral	Day 1, then daily oral maintenance

B12 Injection Standard Regimen (from Adams & Victor's Neurology):

Loading: 1000 mcg cyanocobalamin or hydroxocobalamin IM daily for several days
Consolidation: Weekly for 1 month
Maintenance: Monthly for life (in pernicious anemia/permanent deficiency)
For nutritional/borderline deficiency: 500-1000 mcg oral daily is acceptable for maintenance

5. Conditions Where Both Are Specifically Indicated Together

Pregnancy with severe anemia

Most common scenario in Indian clinical practice
Second and third trimester: FCM preferred over oral iron; B12 supplementation essential
Oral iron often fails due to GI intolerance and hepcidin suppression

Post-bariatric surgery

Gastric bypass removes the site of intrinsic factor secretion (stomach)
Results in permanent B12 malabsorption requiring lifelong IM B12
Also causes iron malabsorption (bypasses duodenum/upper jejunum) - IV FCM often needed

Hemodialysis patients (ALOHA Trial - NCT04627181)

Active RCT at CMC Vellore studying FCM IV + Hydroxycobalamin IM in anemic HD patients
Phase 4, factorial design to determine if combination improves Hb more than either alone

Pernicious anemia with concurrent iron deficiency

Autoimmune gastritis → intrinsic factor loss (B12 malabsorption) + achlorhydria (iron malabsorption)
Both iron and B12 therapy required

Cancer-associated anemia (LMIC guidelines - PMID 37969669)

FCM + B12 + folate combination recommended in resource-limited settings for mixed nutritional anemia

Summary Table

Correlation	Clinical Significance
Co-existing deficiencies	Common in malabsorption, pregnancy, vegans, bariatric surgery, HD
FCM triggers B12/folate consumption	Treat both before/alongside to avoid unmasking deficiency
Masked normocytic MCV	Combined deficiency hides each other - check both in unexplained normocytic anemia
Safe to give together	Different routes, no pharmacokinetic interaction
Hemodialysis	ALOHA trial testing combination (CMC Vellore)
Pernicious anemia	Autoimmune gastritis impairs both iron and B12 absorption
Post-bariatric	Permanent need for IV iron + lifelong IM B12
Pregnancy	FCM + B12 + folate is effective single-visit treatment for severe anemia

Sources:

Adams & Victor's Principles of Neurology, 12e (B12 treatment regimen)
Goldman-Cecil Medicine, 2-Vol (IV iron therapy)
Harrison's Principles of Internal Medicine, 22e (Ch. 102 - Iron deficiency)
PMID 36438538 - FCM + B12 + folate in severe anemia in pregnancy, India
PMC12702285 - FCM effect on B12/folate post-infusion (prospective observational)
ALOHA Trial NCT04627181 - FCM + Hydroxycobalamin in HD patients (CMC Vellore)

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