🍋 C-Vitamin Series — Water-Soluble Antioxidant

Vitamin C (Ascorbic Acid)
Clinical Dose Calculator

WHO/ICMR-aligned dosing for scurvy, surgical wound healing, iron co-therapy, sepsis IV protocols, and burns. All routes and populations.

WHO / ICMR Guidelines Oral · IV Paediatric & Adult Burn & Sepsis Protocols ⚠️ Screen G6PD before High-Dose IV
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G6PD & Renal Safety Warning
High-dose IV Vitamin C (>15 g/dose) can cause haemolysis in G6PD-deficient patients. Mandatory G6PD screening before IV protocols. In CKD or nephrolithiasis history, doses >1000 mg/day may cause calcium-oxalate kidney stones.
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Vitamin C Dose Calculator

WHO / ICMR / CITRIS-ALI / Indian Clinical Standards

Step 1 — Clinical Context
DEFICIENCY
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Scurvy Treatment
Adult & Paediatric
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Wound Healing / Burns
Collagen synthesis support
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Iron Absorption
Co-therapy with iron
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Sepsis / ICU (IV)
CITRIS-ALI / Marik protocol
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Maintenance / RDA
Daily oral supplementation
Step 2 — Formulation
Step 3 — Route
Step 4 — Specific Indication
Dose Recommendation
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⚠️ Evidence-based guidance aligned with WHO, ICMR, and CITRIS-ALI trial data. Renal and G6PD status must be assessed before high-dose therapy. Always apply clinical judgement.
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Vitamin C (Ascorbic Acid) — Complete Clinical Reference

Pharmacokinetics, scurvy protocols, wound healing, iron co-therapy, high-dose IV, renal oxalosis, and G6PD risks.

1. Pharmacokinetics of Ascorbic Acid

Vitamin C (L-ascorbic acid) is a water-soluble six-carbon lactone that humans cannot synthesise de novo due to the absence of the enzyme L-gulonolactone oxidase. This makes dietary or supplemental intake mandatory. At physiological doses (up to 200 mg/day), intestinal absorption approaches 70–90% via sodium-dependent vitamin C transporters (SVCT1 and SVCT2) in the duodenum and jejunum. This is where a key clinical principle emerges: absorption is saturable and dose-dependent.

At oral doses above 1000 mg, bioavailability drops below 50%, with surplus excreted unchanged in urine. This plateau limits the utility of very high oral doses in clinical practice. In states of severe oxidative stress — sepsis, major burns, post-cardiac surgery — tissue Vitamin C levels plummet, and only parenteral (IV) administration can reliably replete plasma and tissue concentrations to pharmacological levels.

ParameterValueClinical Significance
Plasma half-life~10–20 days (physiological)Deficiency develops in 4–6 weeks of zero intake
Plasma saturation~70 µmol/L at 200 mg/day oralHigher oral doses do not raise plasma levels proportionally
Oral bioavailability at 1000 mg~50%Divided doses improve total absorption
IV bioavailability~100%Required for pharmacological (>1 mmol/L) plasma levels
Primary metabolismOxalate (via 2-keto-gulonate)Urinary oxalate rises significantly above 1000 mg/day
Protein bindingNegligibleFreely distributed; crosses placenta

2. Scurvy — Indian Clinical Picture and Treatment Protocols

Scurvy is caused by chronic Vitamin C deficiency, defined as plasma ascorbate below 11 µmol/L. Despite being considered a historical disease, scurvy remains clinically relevant in India among the elderly living alone, chronic alcoholics, patients with tea-and-toast diets, children with autism-related food aversions, and patients on prolonged TPN without Vitamin C supplementation.

Pathophysiology

The biochemical basis of scurvy is the failure of prolyl hydroxylase and lysyl hydroxylase — both Vitamin C-dependent enzymes — to hydroxylate procollagen. Without these hydroxylations, collagen triple helices cannot form stable cross-links, producing structurally weak connective tissue throughout the body. This manifests as vascular fragility (perifollicular haemorrhage), impaired wound healing, and osteoporosis.

Clinical Recognition

The hallmarks of scurvy progress in a predictable sequence. Early: follicular hyperkeratosis and "corkscrew hairs" around hair follicles on the thighs and buttocks. Intermediate: perifollicular haemorrhage and "woody oedema" of the lower limbs. Advanced: scorbutic gingivitis (friable, purple-blue gums bleeding with minimal provocation), subperiosteal haemorrhage causing bone pain, and large echymoses. In children, the classic "frog-leg" posture from painful lower-limb haemorrhages is pathognomonic.

RDA (Adult)
75–90 mg/day
Dietary maintenance
Mild Deficiency
500 mg/day
Divided doses × 1 month
Confirmed Scurvy
1000 mg/day
× 1 month; or IV if severe
Sepsis / Burns
6 g/day IV
1.5 g q6h × 4 days

Standard Replacement Protocol

PopulationDoseRouteDurationNotes
Confirmed Scurvy — Adult500–1000 mg/dayOral (divided doses)≥1 month500 mg BD or 250 mg QDS
Severe/Hospitalised Adult1000 mg/dayIV or OralUntil symptoms resolveIV if GI absorption impaired
Paediatric Scurvy100–300 mg/dayOral (divided doses)2–4 weeksWeight-based: ~10 mg/kg/day; max 300 mg
Subclinical / At-Risk Adult250–500 mg/dayOralOngoing until diet improvedElderly, alcoholics, institutional patients
Prophylaxis (smokers)+35 mg/day above RDAOralOngoingICMR: smokers need 110–125 mg/day minimum
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Speed of Recovery — A Diagnostic Clue
Clinical response to Vitamin C in scurvy is dramatic and rapid. Spontaneous bleeding stops within 24 hours. Muscle and joint pain resolves within 48–72 hours. The prompt response to supplementation is itself diagnostically reassuring when plasma levels are unavailable. Associated iron-deficiency anaemia corrects more slowly and requires concurrent iron therapy over weeks.
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Clinical Pearl — Ascorbic Acid Degradation in India's Climate
Vitamin C is highly sensitive to heat, light, and air. Tablets or syrups that have turned brown or orange have undergone oxidation to dehydroascorbic acid, which is further hydrolysed to inactive diketo-L-gulonic acid. Advise patients to store Vitamin C products in cool, dark conditions — and to discard any discoloured preparations.

3. Vitamin C in Wound Healing, Burns, and Surgical Recovery

Ascorbic acid is the non-negotiable co-factor for both prolyl hydroxylase and lysyl hydroxylase, the enzymes that introduce stability-conferring hydroxyl groups into procollagen chains. Without these modifications, collagen cannot form the triple-helical structure required for tensile strength. In any healing wound, Vitamin C is being consumed rapidly at the site — local tissue levels often become depleted even when systemic plasma levels appear normal.

Burns — A Special High-Demand Scenario

Thermal injury creates massive oxidative stress and dramatically increases metabolic demand for Vitamin C — requirements can reach 10–20 times the RDA. Large burns cause a capillary leak syndrome in which Vitamin C, as an antioxidant, helps protect vascular endothelial integrity and may reduce resuscitation fluid volumes when given as high-dose IV within the first 24 hours.

ScenarioDoseRouteDurationNotes
Post-operative wound healing500 mg dailyOralUntil wound closedElective surgery — pre-load if malnourished
Major surgery / large wounds1000–2000 mg dailyOralUntil secondary intention closureDivided into BD–TDS doses
Minor-to-moderate burns (<20% BSA)1000–2000 mg dailyOral or IV7–14 daysMaintain until re-epithelialisation
Major burns (≥20% BSA)66 mg/kg/hour × 24hIV infusionFirst 24 hours onlyNiwa protocol; monitor urine output hourly
Chronic non-healing wounds500–1000 mg dailyOral4–8 weeks; reassessAlways check serum Vit C — subclinical deficiency common
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Screen for Subclinical Deficiency Before Major Surgery
Plasma Vitamin C below 11 µmol/L (deficiency) is found in up to 30–50% of surgical patients in some Indian series, particularly in those with a poor vegetarian diet, alcohol use, or prolonged hospitalisation. Pre-operative Vitamin C supplementation for 7–10 days before elective surgery may significantly improve wound outcome.

4. Synergistic Role in Iron Deficiency Anaemia

Iron deficiency anaemia is the single most common micronutrient deficiency in India, affecting an estimated 50–60% of women of reproductive age. Vitamin C is one of the most potent enhancers of non-haem iron absorption known. Its mechanism is dual: it reduces ferric iron (Fe³⁺) — the oxidised, insoluble form found in plant foods — to ferrous iron (Fe²⁺), which is the only form transported across intestinal epithelium by DMT-1 (Divalent Metal Transporter 1). Simultaneously, Vitamin C chelates iron in the acidic gastric environment, keeping it soluble and preventing inhibition by phytates, oxalates, and tannins ubiquitous in Indian cereal and pulse-heavy diets.

Clinical Co-administration Protocol

Elemental Iron DoseVitamin C Co-doseTimingNotes
30–60 mg elemental iron200 mgSame dose; fasting or mid-mealStandard paediatric iron co-therapy
60–100 mg elemental iron200–500 mgSimultaneously; avoid tea/milk ±1hAdult iron deficiency anaemia
100–200 mg elemental iron500 mgSimultaneously; empty stomach preferredSevere anaemia; post-partum
IV iron (any dose)Not required—IV iron bypasses GI absorption — Vit C co-therapy has no role
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Practical Dietary Advice for Indian Patients
A glass of fresh lemon water, a small guava, or 2–3 pieces of amla with every iron tablet is equivalent to a 200–500 mg Vitamin C co-dose. This is culturally accessible, inexpensive, and highly effective. Conversely, a cup of chai (tea) taken within 1 hour of iron reduces absorption by up to 60% — advise patients specifically to avoid tea and coffee peri-dosing.

5. High-Dose IV Vitamin C — Sepsis and Oncology Protocols

Intravenous Vitamin C (IVC) has emerged as an area of active investigation in critical care and oncology. The rationale is pharmacological: oral Vitamin C can achieve plasma levels of only 70–100 µmol/L at saturation, but IV infusion can achieve plasma levels of 10–20 mmol/L — concentrations 100–200 times higher that exert pro-oxidant, anti-inflammatory, and immunomodulatory effects not achievable by oral therapy.

Sepsis and ICU — CITRIS-ALI Protocol

The CITRIS-ALI randomised controlled trial (2019) demonstrated that IV Vitamin C 200 mg/kg/day (in 4 divided doses of 50 mg/kg q6h) in ARDS patients significantly reduced biomarkers of inflammation and organ injury. The "Marik Protocol" (Vitamin C + Thiamine + Hydrocortisone) has been widely discussed, though subsequent trials have produced mixed results — institutional protocols should be followed.

ProtocolDoseRouteDurationNotes
CITRIS-ALI (Sepsis/ARDS)1.5 g q6h (6 g/day)IV infusion over 30–60 min4 daysDilute in 100 mL NS; G6PD screen mandatory
Marik Protocol adjunct1.5 g q6hIV4 days or ICU dischargeAdd thiamine 200 mg BD + hydrocortisone per protocol
Burns — Niwa Protocol66 mg/kg/hourContinuous IVFirst 24 hours onlyReduces resuscitation fluid; monitor UO hourly
Palliative / Oncology IVC15–100 gSlow IV over 60–90 min2–3×/week; variableG6PD screen mandatory; renal function monitoring
Post-cardiac surgery oxidative stress1000–3000 mg/dayIV or Oral5–7 daysReduces AF incidence in some trials
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Mandatory G6PD Screening Before High-Dose IV
High-dose IV Vitamin C acts as a pro-oxidant at pharmacological plasma concentrations. In patients with G6PD deficiency — prevalent in approximately 3–15% of the Indian male population depending on region — this pro-oxidant activity can overwhelm erythrocyte antioxidant defence, precipitating acute haemolytic anaemia. G6PD testing is mandatory before any IV protocol exceeding 15 g/dose. Standard oral Vitamin C doses are generally safe.

6. Toxicity, Contraindications, and Renal Safety

Vitamin C has a favourable safety profile at nutritional and moderate supplemental doses. However, high-dose use introduces specific risks that the Indian clinician must recognise, particularly given the high background prevalence of urinary stone disease and G6PD deficiency.

Renal Oxalosis and Nephrolithiasis

Approximately 40% of urinary oxalate is derived from ascorbate catabolism. At doses above 1000 mg/day, urinary oxalate excretion increases significantly and in susceptible individuals can precipitate calcium-oxalate urolithiasis. Patients with CKD, a personal or family history of oxalate stones, or hyperoxaluria should not receive chronic high-dose oral Vitamin C without specialist guidance. In acute settings (burns, sepsis), the short duration of high-dose IV is generally acceptable.

Risk / InteractionThreshold / ContextManagement
Calcium-oxalate nephrolithiasis>1000 mg/day chronic oralLimit to ≤500 mg/day in stone history; high fluid intake
G6PD haemolysis (IV)>15 g/dose IVMandatory G6PD screen before high-dose IV protocol
Urine glucose (dipstick) — false negativeAny high doseUse glucose oxidase method; warn diabetic patients
Occult blood (faecal) — false negativeAny high doseDiscontinue 3 days before faecal OBT testing
Iron overload (hereditary haemochromatosis)Any supplemental doseAvoid supplemental Vitamin C — enhances iron absorption further
Nausea / GI upset>1000 mg single oral doseDivide doses; take with food; switch to buffered (sodium ascorbate)
Warfarin interactionHigh-dose chronicMonitor INR — large doses may reduce warfarin anticoagulation effect

7. Vitamin C in Pregnancy and Lactation

Vitamin C requirements increase modestly in pregnancy and lactation. The ICMR (2020) recommends 80 mg/day in pregnancy and 85 mg/day in lactation, well above the non-pregnant adult RDA of 65–75 mg/day. Standard prenatal multivitamins contain adequate amounts. Supplemental Vitamin C is safe at nutritional doses during pregnancy; however, very high doses (above 2000 mg/day) are not recommended due to theoretical risk of conditioning the foetus to high Vitamin C turnover and a "rebound scurvy" effect in the neonate.

ContextDoseRouteNotes
Normal pregnancy (RDA)80 mg/dayOral (prenatal vitamin)ICMR 2020 recommendation
Lactation (RDA)85 mg/dayOralBreast milk Vitamin C reflects maternal intake
Pre-eclampsia prevention1000 mg/dayOralEvidence mixed; consult current obstetric guidelines
Scurvy in pregnancy500–1000 mg/dayOral or IVSame protocol as non-pregnant; safe at therapeutic doses
Maximum safe in pregnancy2000 mg/day (UL)OralDo not exceed — neonatal rebound scurvy risk

8. Frequently Asked Questions

What is the standard dose of Vitamin C for scurvy in adults?
WHO recommends 500–1000 mg daily in divided doses for confirmed adult scurvy, for a minimum of 1 month. Severe or hospitalised patients should receive 1000 mg/day orally or IV. Clinical response is rapid: spontaneous bleeding typically stops within 24 hours and joint pain resolves within 48–72 hours. Concurrent iron supplementation is usually required for the associated iron-deficiency anaemia.
Can Vitamin C cause kidney stones?
Yes, at high doses. Ascorbate is metabolised to oxalate, and at doses exceeding 1000 mg/day, urinary oxalate excretion rises significantly. In patients with a history of calcium-oxalate nephrolithiasis, CKD, or hyperoxaluria, chronic high-dose oral Vitamin C substantially increases stone risk. These patients should generally be limited to no more than 500 mg/day, with high fluid intake. The short-term IV use in burns and sepsis is generally acceptable due to the brief duration.
How much Vitamin C should I take with iron supplements?
200–500 mg of Vitamin C should be co-administered with each dose of oral iron. This reduces ferric (Fe³⁺) to ferrous (Fe²⁺) iron, which is the absorbable form, and chelates iron to prevent inhibition by phytates and tannins common in Indian diets. Practical advice: one guava, a small amla, or a glass of fresh lemon water taken with the iron tablet provides an effective and accessible Vitamin C dose. Avoid tea, coffee, and milk within 1 hour of iron dosing.
What is the IV Vitamin C dose for sepsis?
The CITRIS-ALI trial used 1.5 g IV every 6 hours (total 6 g/day) for 4 days. The Marik Protocol combines this with thiamine 200 mg IV BD and hydrocortisone 50 mg IV q6h. Dilute each IV dose in 100 mL NS and infuse over 30–60 minutes. G6PD screening is mandatory, and renal function should be monitored throughout. Institutional ICU protocols should be followed, as subsequent trials have produced variable results.
Is high-dose Vitamin C safe in G6PD deficiency?
No — high-dose IV Vitamin C acts as a pro-oxidant at pharmacological plasma concentrations and can precipitate acute haemolytic anaemia in patients with G6PD deficiency. G6PD deficiency affects approximately 3–15% of Indian males depending on the region. G6PD screening is mandatory before IV protocols exceeding 15 g/dose. Standard oral Vitamin C at nutritional doses (up to 200 mg/day) is generally safe in G6PD-deficient patients.
Does Vitamin C interfere with laboratory tests?
Yes. High Vitamin C levels cause clinically important lab interferences: (1) False-negative urine glucose dipstick results — the reducing property of ascorbate competes with the glucose oxidase reaction; diabetic patients relying on dipstick monitoring must use glucose oxidase-specific strips. (2) False-negative faecal occult blood tests — Vitamin C should be stopped at least 3 days before any occult blood testing. Inform the laboratory of high-dose Vitamin C use when ordering these tests.
What is the Vitamin C dose for burns?
For major burns (≥20% BSA), the Niwa Protocol uses 66 mg/kg/hour as a continuous IV infusion for the first 24 hours only — this may reduce total resuscitation fluid requirements. For minor-to-moderate burns and ongoing wound recovery, 1000–2000 mg/day orally or IV is used until re-epithelialisation. Always monitor urine output hourly during high-rate IV infusion.
Disclaimer: This calculator provides evidence-based guidance aligned with WHO Scurvy Guidelines, ICMR 2020 RDA recommendations, CITRIS-ALI trial data, and published Indian clinical literature. Doses must be verified against current prescribing information and adjusted for individual patient factors including renal function and G6PD status. This tool is for use by qualified healthcare professionals and does not replace clinical judgement or direct medical consultation.