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Summary Table

Category	Details
Risk Factors	Elderly living alone, chronic alcoholism, psychiatric illness, food insecurity, infants fed exclusively boiled or evaporated milk, restrictive diets (no fruits/vegetables), malabsorption syndromes, patients on chronic hemodialysis, smokers (increased vitamin C turnover)
Etiology	Deficiency of ascorbic acid (vitamin C) due to inadequate dietary intake; body stores typically deplete after 1 to 3 months of near-zero intake
Patient Presentation	Fatigue, malaise, myalgia, followed by gingival bleeding, easy bruising, poor wound healing, and joint pain
Classic Physical Exam	Perifollicular hemorrhages with corkscrew (coiled) hairs, swollen and spongy gums that bleed easily (especially in dentate patients), ecchymoses, petechiae, subperiosteal hemorrhage in children, Scorbutic rosary (costochondral beading in pediatric cases)
Key Diagnostic Results	Serum ascorbic acid level < 0.2 mg/dL (11.4 micromol/L); clinical diagnosis supported by dietary history; imaging in children may show Wimberger ring sign, Frankel line, and Trummerfeld zone
Management	Oral ascorbic acid supplementation (500 to 1000 mg/day in divided doses for adults); dietary counseling; symptoms improve within days to weeks
Keywords	"Corkscrew hairs," "perifollicular hemorrhages," "swollen bleeding gums," "poor wound healing," "diet lacking fruits and vegetables," "Scorbutic rosary," "subperiosteal hemorrhage in a child"

1. Pathophysiology

Vitamin C is an essential cofactor for prolyl hydroxylase and lysyl hydroxylase, the enzymes responsible for hydroxylation of proline and lysine residues during collagen synthesis. Without adequate ascorbic acid, the resulting collagen molecules are structurally unstable and cannot form proper triple-helix configurations. This defective collagen is the central mechanism behind virtually every manifestation of scurvy: blood vessels become fragile (leading to hemorrhage), wound healing stalls, and connective tissue throughout the body weakens.

The bleeding tendency in scurvy is not a coagulopathy in the traditional sense. Platelet count and coagulation cascades (PT, PTT) are typically normal. Instead, the hemorrhagic manifestations arise from loss of vascular structural integrity due to defective collagen in capillary basement membranes. This is why the bleeding pattern is characteristically perivascular: perifollicular petechiae around hair follicles, gingival hemorrhage, and subperiosteal bleeding.

Vitamin C also functions as a potent antioxidant and plays a role in iron absorption (by reducing ferric iron to ferrous iron in the gut) and in the synthesis of carnitine and certain neurotransmitters (norepinephrine, serotonin). This explains the early constitutional symptoms of fatigue and irritability that precede the more dramatic hemorrhagic signs. Prolonged deficiency can contribute to iron-deficiency anemia both through impaired absorption and through chronic blood loss from widespread capillary hemorrhage.

In children, the skeletal findings are prominent because vitamin C is critical for osteoid formation. Growing bones require constant collagen deposition; when this fails, the periosteum separates from underlying bone due to subperiosteal hemorrhage, and the zone of provisional calcification becomes irregular. The child presents with bone pain, pseudoparalysis (refusal to move limbs), and a characteristic frog-leg position.

2. Classification and Clinical Manifestation

Phase	Timeframe	Clinical Features
Early / Nonspecific	1 to 3 months	Fatigue, malaise, irritability, anorexia, vague myalgia and arthralgia
Moderate / Dermatologic-Mucosal	3 to 6 months	Perifollicular hemorrhages, corkscrew hairs, follicular hyperkeratosis, gingival swelling and bleeding (only in dentate individuals), easy bruising, ecchymoses
Severe / Systemic	Beyond 6 months	Large ecchymoses, hemarthrosis, subperiosteal hemorrhage, poor wound healing or dehiscence of previously healed wounds, loose teeth, secondary infection of gums, anemia (iron-deficiency or combined)
Pediatric Presentation (Moeller-Barlow Disease)	Variable	Irritability, pseudoparalysis and frog-leg posture (due to pain), Scorbutic rosary (enlarged costochondral junctions), subperiosteal hemorrhage of long bones, paradoxical tenderness with handling

Clinical Manifestation

Finding	Pathophysiologic Basis
Corkscrew hairs	Defective collagen in hair follicle connective tissue causes abnormal coiling
Perifollicular hemorrhage	Capillary fragility around follicles from weakened basement membranes
Gingival bleeding and swelling	Fragile gingival vasculature; absent in edentulous patients because teeth provide the mechanical irritation that triggers hemorrhage in weakened tissue
Poor wound healing / reopening of old scars	New collagen cannot be synthesized; even previously deposited collagen turns over and degrades
Subperiosteal hemorrhage (children)	Fragile periosteal vessels rupture; periosteum lifts off the cortex
Scorbutic rosary	Subluxation and swelling at costochondral junctions from defective cartilage matrix

3. Diagnostic Workup

Test	Role	Key Findings
Serum ascorbic acid level	Best initial test	< 0.2 mg/dL (11.4 micromol/L) confirms deficiency; levels < 0.6 mg/dL suggest depletion
Leukocyte (buffy coat) ascorbic acid level	Most accurate test (reflects tissue stores)	More reliable than serum level as it represents intracellular vitamin C status; not widely available
Complete blood count	Supportive	May show normocytic or microcytic anemia (from chronic blood loss or impaired iron absorption)
Coagulation studies (PT, PTT, INR)	Rule out coagulopathy	Typically normal in scurvy; this helps distinguish it from bleeding disorders
X-ray of long bones (pediatric)	Supportive in children	Wimberger ring sign (sclerotic ring around epiphyses), Frankel line (dense zone of provisional calcification), Trummerfeld zone (lucent zone beneath Frankel line), subperiosteal elevation from hemorrhage
Skin biopsy	Rarely needed	Perifollicular hemorrhage and corkscrew hair changes

In practice, scurvy is overwhelmingly a clinical and dietary diagnosis. The classic exam vignette presents a patient with a clearly inadequate diet (alcoholic male living alone, a child on restrictive or unusual diet, an elderly person eating only tea and toast) combined with the hallmark physical findings of perifollicular hemorrhage and corkscrew hairs.

The best initial test on an exam is serum ascorbic acid level, which is quick and accessible. However, serum levels fluctuate with recent intake and do not reliably reflect total body stores. The leukocyte ascorbic acid level (buffy coat assay) is the most accurate measure of tissue-level vitamin C status, but it is seldom ordered in real-world practice and is primarily a test-taking distinction.

A critical diagnostic reasoning point: when a vignette describes a bleeding patient with normal PT, PTT, and platelet count, this should immediately trigger you to think beyond coagulation factor deficiencies and thrombocytopenia. The combination of mucocutaneous bleeding plus normal coagulation studies plus a poor diet points directly to scurvy. Test-writers use the normal coagulation panel as a deliberate clue to steer you away from hemophilia, von Willebrand disease, and ITP.

In pediatric cases, the radiographic findings are high-yield. The Frankel line (a dense white line at the metaphysis representing calcified but non-resorbed cartilage) and the Trummerfeld zone (a lucent band just proximal to it representing inadequate osteoid) together create a characteristic layered appearance. The Wimberger ring sign refers to a sharply demarcated sclerotic ring around the epiphyseal ossification center. These findings, combined with subperiosteal hemorrhage, are pathognomonic in the right clinical context.

4. Management and Treatment

Setting	Intervention	Details
Acute adult treatment	Oral ascorbic acid	500 to 1000 mg/day in 2 to 3 divided doses for at least 1 month, then taper to maintenance
Maintenance / Prevention (adults)	Oral ascorbic acid	75 to 90 mg/day (recommended daily allowance); smokers need an additional 35 mg/day
Pediatric treatment	Oral ascorbic acid	100 to 300 mg/day in divided doses for at least 2 weeks, then maintenance per age-appropriate RDA
Dietary counseling	Increase dietary sources	Citrus fruits, bell peppers, strawberries, broccoli, tomatoes, potatoes
Concurrent iron-deficiency anemia	Oral iron supplementation	Vitamin C enhances iron absorption; co-administration is synergistic
Severe or symptomatic anemia	Packed red blood cell transfusion	Only if hemodynamically significant

Acute treatment centers on prompt oral ascorbic acid replacement. The typical adult regimen is 500 to 1000 mg per day divided into two or three doses, continued for a minimum of one month. Clinical improvement is rapid: fatigue and malaise begin to resolve within 24 to 48 hours, and gingival symptoms and skin hemorrhages start improving within one to two weeks. Complete healing of dermatologic and mucosal findings usually takes one to three months.

For the "next best step" logic on an exam, the answer is almost always start oral vitamin C supplementation. Parenteral (IV) ascorbic acid is reserved for patients who cannot take oral medications (severe malabsorption, critically ill patients, or those with gastrointestinal pathology preventing absorption). Exam questions rarely test parenteral dosing; the oral route is the expected answer.

Dietary counseling is a required component of management and is often tested as part of the long-term plan. Even after symptoms resolve with supplementation, the patient must be educated on maintaining adequate vitamin C intake through diet to prevent recurrence.

When concurrent iron-deficiency anemia is present, both vitamin C and iron should be supplemented simultaneously. Vitamin C reduces ferric iron ($Fe^{3+}$) to ferrous iron ($Fe^{2+}$) in the duodenum, facilitating absorption. This biochemical synergy is testable.

There are no notable drug contraindications to standard vitamin C supplementation at therapeutic doses. At very high doses (>2 g/day), there is a theoretical increased risk of oxalate nephropathy and kidney stones in predisposed individuals, but this is rarely relevant at the doses used for scurvy treatment. Patients with glucose-6-phosphate dehydrogenase (G6PD) deficiency should avoid extremely high intravenous doses, as this can provoke hemolysis, though this is an uncommon testing scenario.

5. Differential Diagnosis and Distractors

Differential Diagnosis	Why It Looks Similar	Key Discriminator
Henoch-Schonlein Purpura (IgA Vasculitis)	Purpura and joint pain in a child	HSP purpura is palpable and concentrated on the lower extremities and buttocks; scurvy has perifollicular hemorrhages and corkscrew hairs with a poor diet history
Immune Thrombocytopenic Purpura (ITP)	Petechiae and easy bruising	ITP shows a low platelet count; scurvy has normal platelets and normal coagulation studies
Hemophilia A or B	Bleeding tendency, hemarthrosis	Hemophilia shows a prolonged PTT with normal PT; scurvy has entirely normal coagulation studies
Von Willebrand Disease	Mucocutaneous bleeding	Prolonged bleeding time or abnormal PFA-100, low vWF activity; scurvy has normal platelet function
Child abuse / Non-accidental trauma	Subperiosteal hemorrhage and bruising in a child	Abuse shows fractures in various stages of healing, inconsistent history, retinal hemorrhages; scurvy shows characteristic radiographic findings (Frankel line, Wimberger sign) and dietary deficiency
Vitamin K Deficiency	Bleeding, bruising	Vitamin K deficiency causes prolonged PT/INR from impaired synthesis of factors II, VII, IX, X; scurvy has normal coagulation
Rickets (Vitamin D Deficiency)	Skeletal findings in children, costochondral beading (Rachitic rosary)	Rickets shows widened, cupped, and frayed metaphyses with low calcium/phosphorus and elevated alkaline phosphatase; scurvy shows dense metaphyseal lines and subperiosteal hemorrhage
Ehlers-Danlos Syndrome	Easy bruising, poor wound healing, connective tissue fragility	EDS is a genetic collagen disorder present from birth with joint hypermobility and skin hyperextensibility; scurvy is acquired and tied to dietary history

6. Traps and High-Yield Pearls

The most common trap on scurvy questions is not recognizing the dietary history as the critical clue. Vignette writers will often bury a line about the patient's diet ("eats only canned food," "hasn't eaten fresh produce in months," "drinks alcohol daily and eats minimally") among a long list of presenting complaints. Students who skip over this social history element and focus only on the bleeding will be tempted to pick a coagulopathy or platelet disorder, especially since scurvy appears infrequently on exams and is not top of mind.

Another common pitfall is confusing Scorbutic rosary with Rachitic rosary. Both produce costochondral beading in children, but the underlying mechanisms and associated findings are entirely different. The exam may present both as answer choices for a child with skeletal abnormalities, and the discriminator is the presence of hemorrhagic findings (scurvy) versus metabolic bone changes with low calcium and elevated alkaline phosphatase (rickets).

In pediatric vignettes, scurvy can be mistaken for child abuse because of the subperiosteal hemorrhage and widespread bruising. The key discriminator is the radiographic pattern (Frankel line, Trummerfeld zone, Wimberger ring sign) combined with dietary history and the absence of inconsistent trauma histories or retinal hemorrhages.

The core competency being tested is threefold: first, recognizing that normal coagulation studies in a bleeding patient should redirect your differential away from factor deficiencies and toward vascular or connective tissue causes; second, linking the clinical findings to a dietary and social history that explains the pathophysiology; and third, understanding that defective collagen synthesis is the unifying mechanism behind all the seemingly disparate manifestations of this disease.

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