Patient-Completed Screening Instrument for Functional Disability in the Elderly
A Case of Scurvy in an Elderly Patient
-
Upload
fathia-rachmatina -
Category
Documents
-
view
216 -
download
0
Transcript of A Case of Scurvy in an Elderly Patient
-
7/27/2019 A Case of Scurvy in an Elderly Patient
1/8
A Case of Scurvy in an Elderly Patient
Authors:
Panagiotis H. Panagiotakis, MD, and Kathryn A. Peterson, MD
CASE PRESENTATION
A 70-year-old man was brought to the emergency room by his neighbor, who reported a 10-
day history of progressive fatigue, leg pain, and generalized weakness. The patient had
suffered an ischemic stroke 7 months before and was dependent on his neighbor for his daily
care. His past medical history was significant for hypertension. His caretaker also commented
on the patients decline in function during the last month, noting some bloody stools,
shortness of breath, easy bruising, leg swelling, and a recent red rash on his arms and
legs. The patient had no known allergies, and his daily medications were aspirin 81 mg
orally, lansoprazole 30 mg orally before meals, and hydrochlorothiazide 25 mg orally. He
denied use of tobacco or illicit drugs. He drank 1-2 cans of beer per day. The patient was
admitted to the Medicine service.
The patients initial vital signs were: heart rate 100 beats/min, blood pressure 110/65 mm Hg,
respiratory rate 18 breaths/min, and temperature 36.8 degrees C. His height was 1.88 m, and
he weighed 67 kg (body mass index = 19). Physical examination revealed lethargy, cachexia,
left hemiparesis, poor dentition, gingival erythema, and pitting edema (2+). The skin
examination showed small petechiae in the upper and lower extremities and large
ecchymoses below the knees bilaterally. He was found to be anemic (hemoglobin 9.1 g/dL,
mean corpuscular volume 88) with normal differential, platelet count, prothrombin time (PT),
and partial thromboplastin time (PTT). His electrolytes (sodium, potassium, calcium,
magnesium, phosphate) were all within normal limits. His chest x-ray was normal, and acomputed tomography scan of the brain failed to identify recent lesions. Stool specimen was
positive for blood. Urinalysis revealed a urinary tract infection, and appropriate antibiotic
therapy was started. Iron and ferritin levels were low normal. B12 and folate levels were also
normal. Albumin count was 3.0 g/dL. Work-up for hepatitis, hemolysis, and vasculitis were
negative. Idiopathic thrombocytopenic purpura and thrombotic thrombocytopenic purpura
were ruled out since the PT and PTT were normal. Doppler ultrasonography of the lower
extremities was negative for deep vein thrombosis.
-
7/27/2019 A Case of Scurvy in an Elderly Patient
2/8
The patient was referred to a gastroenterologist for endoscopy. Esophagogastroduodenoscopy
(EGD) revealed mild esophagitis at the gastro-esophageal junction (Los Angeles class A) and
normal stomach and duodenum. Colonoscopy revealed diverticulosis of the sigmoid colon
and internal hemorrhoids. A source of bleeding was not identified.
Considering the patients poor nutritional status, a serum ascorbic acid (vitamin C) level was
ordered. It was found to be less than 0.02 mg/dL (normal = 0.2-2.0 mg/dL). The diagnosis of
scurvy and malnutrition was made. We re-examined the patient and identified corkscrew-like
hairs. A dietary history showed that the patients diet consisted entirely of bread, cheese,
pasta, canned meatballs, and beer. The patient was started on a high-protein diet with vitamin
C supplementation (1 g daily). His improvement was dramatic. After the 10th day of his
hospitalization, the patient was back at his baseline with total resolution of his fatigue,
extremity pain, generalized weakness, and skin lesions. He was discharged home under the
care of a visiting nurse. His hemoglobin was 12.8 g/dL at his 1-month follow-up visit.
DISCUSSION
Hypovitaminosis C or scurvy (called the despicable disease)1 has been described for
centuries, first in 1541 by a Dutch physician named Echthius in Cologne, Germany, who
thought it was an infectious disease. In 1540, the French explorer Jacques Cartier was told of
a remedy for scurvy made of pine tree needles from Native Americans in Canada. The first
English reference to the disease appeared in the Oxford English Dictionary in 1565.
Scurvy was recognized as an important problem beginning in the 15th century, when it
ravaged crews during lengthy seafaring voyages. The Portuguese sailor Vasco da Gama
described 100 of his 160 crew members as having developed severe lassitude and swelling of
legs, hands, and gums, resulting in fatality.
Scurvy was not, however, limited to sailors. Cases were described during the Peloponnesian
war, the Crusades, the Napoleonic wars, the American Civil War, the exploration of the
Poles, the Irish famine, the Mormon trail (Black-Leg disease), and even among soldiers in
World War I.2-7
Two physicians who played a significant role in decreasing mortality from scurvy were John
Woodall and James Lind. In 1617, Woodall wrote The Surgeons Mate, which described the
disease and listed lemon juice as the cure. Woodall was responsible for persuading the EastIndia Company to give lemon juice to its sailors.4 In 1753, Lind published The Treatise on
-
7/27/2019 A Case of Scurvy in an Elderly Patient
3/8
the Scurvy.8He was a naval surgeon in the British Royal Navy and described his clinical trial
on board the HMS Salisbury. On May 20, 1747, he divided 12 sailors suffering from scurvy
into six groups of two, and he treated each group with a different remedy. Only the two
sailors given two oranges and one lemon daily improved. Unfortunately, it took 41 years
before his recommendations were adopted. The British used lime juice instead of lemon or
orange juice to prevent the disease; thus, the term limeys originated.
Vitamin C is a water-soluble vitamin that was first isolated in 1928 by Hungarian chemist
Albert von Szent-Gyrgyi.3He named it ascorbic acid (for its anti-scorbutic effects) in
1932 and received the Nobel Prize in 1937.5 Humans, other primates, and guinea pigs cannot
synthesize ascorbic acid like other living organisms, and so are dependent on ascorbic acid
from dietary sources. The enzyme L-gluconolactone oxidase, which usually would catalyze
the conversion of L-gluconogammalactone to L-ascorbic acid, is defective due to a mutation
or inborn error in carbohydrate metabolism. Ascorbic acid is a necessary cofactor in the
synthesis of collagen.9During the pro-alpha chain processing in the rough endoplasmic
reticulum of the cell, lysine and proline residues are hydroxylated to hydroxylysine and
hydroxyproline. This is an important step for the collagen fiber cross-linking. The
hydroxylases need vitamin C as a reducing agent and molecular oxygen. In scurvy, collagen
fibers cannot be cross-linked, greatly decreasing the tensile strength of the fiber. This resultsin the breakdown of connective tissue in and around the walls of blood vessels.
Scurvy is characterized by bleeding due to capillary fragility, poor healing of wounds, and, in
children (Cheadle-Mller-Barlow syndrome), bone abnormalities (scurvy rosary).10 The most
characteristic physical finding is the perifollicular hemorrhage, a hyperkeratotic follicle
surrounded by a pink halo. Hairs may acquire a corkscrew appearance. Other manifestations
include purpura, intramuscular hemorrhage, gingival involvement in dentulous patients,
edema, exertional dyspnea,11 and emotional disturbances that can include apathy, depression,
bipolar disorder, and anxiety.12,13Anemia is common and multifactorial, with causes
including hemorrhage into tissues, altered metabolism, deficiencies of folate and iron,
gastrointestinal (GI) blood loss, and intravascular hemolysis.14 Late signs include icterus and
fever, and sudden death can occur.
Other, less common manifestations of scurvy include ocular hemorrhages,15Sjgrens
syndrome,16 femoral neuropathy (resulting from hemorrhage into the femoral
-
7/27/2019 A Case of Scurvy in an Elderly Patient
4/8
sheaths),17 impaired vascular reactivity,18 and arthritis.11 Rare cases of cardiac involvement in
patients with scurvy have been reported.19,20
Lind8 reported the onset of scurvy in sailors after a 1.5-month period at sea and described
lassitude as its early and consistent symptom. Depletion-repletion studies in volunteers using
a vitamin Cfree diet have shown that plasma vitamin C level falls below 0.2 mg/dL in less
than 1 month. At these concentrations, fatigue is usually noted, with physical signs soon
appearing.21,22The recommended daily allowance for vitamin C varies. The Food and
Nutrition Board of the United States National Academy of Sciences recommended
allowances for vitamin C are 75 mg per day for women and 90 mg per day for men. Higher
doses are recommended for smokers, alcoholics, persons with diabetes, and those who are
severely ill. More recent recommendations suggest 120 mg daily.23 Some experts feel that the
level should be as high as 200 mg daily to match the level present in five servings of fruits
and vegetables daily, a diet shown to decrease cancer risk.
Vitamin C intake has been reported to be less than 60 mg per day in 20-30% of U.S.
adults,24 and even lower among many population subgroups. Since the first symptom is
fatigue, a common, nonspecific complaint, subclinical vitamin C deficiency is much more
common than is generally noted.25,26 Population subgroups at risk are the elderly (who
sometimes have tea-and-toast diets), the socially isolated, alcoholics, food
faddists,27,28 patients with psychiatric illness,29 and young children (eating exclusively cows
milk formula).30 Cigarette smokers require increased intake of vitamin C due to lower
vitamin C absorption. Pregnant and lactating women and patients with thyrotoxicosis require
increased intake of vitamin C because of increased utilization. Vitamin C deficiency has
recently been noted in refugees who are dependent on external suppliers for their food and
have limited access to fresh fruits and vegetables.31 Large doses of vitamin C (eg, more than
1 g/day) may increase the risk of kidney stones, particularly oxalate stones. 23
The correct diagnosis of scurvy can be delayed because the disease can mimic disorders such
as vasculitis, systemic bleeding disorders, and deep vein thrombosis; patients with scurvy are
often evaluated for other disorders. Knowledge of the manifestations of scurvy and higher
levels of suspicion of the high-risk groups is important for clinicians to help in prevention.
Taking a patients extensive dietary history can be very helpful; a plasma or leukocyte
vitamin C level finding can confirm the clinical diagnosis. Capillary fragility can be checked
by inflating a blood pressure cuff and observing a patients forearm for petechiae.
-
7/27/2019 A Case of Scurvy in an Elderly Patient
5/8
Treatment of scurvy is simple and effective. The usual dose in adults is 100 mg orally 3-4
times daily until 4 g have been administered, then 100 mg per day. Orally-administered
vitamin C is well absorbed from the GI tract. It can also be given intravenously or
intramuscularly in special circumstances. A diet rich in vitamin C should be initiated
simultaneously.32 Foods rich in vitamin C are citrus fruits (especially grapefruit and lemons)
and vegetables (eg, broccoli, green peppers, tomatoes, cabbage).
Patients respond quickly to oral therapy, and the prognosis is excellent: spontaneous bleeding
ceases within 1 day, muscle and bone pain stop quickly, bleeding and sore gums heal in 2-3
days, and ecchymoses heal within 12 days.
In advanced scurvy, serum bilirubin normalizes in less than 1 week, and anemia is corrected
in 2-4 weeks.32
CONCLUSION
Scurvy is a relatively uncommon diagnosis, but the consequences of a missed diagnosis can
be dire. Clinicians should consider hypovitaminosis C or other nutritional deficiencies in such
high-risk groups as the elderly, those who are socially isolated, alcoholics, food faddists,
patients with psychiatric illness, and young children. With a high level of suspicion,
knowledge of the symptomatology, and a thorough dietary history, the diagnosis can be
easily made. The treatment of scurvy is simple and effective.
The authors report no relevant financial relationships.
References:
REFERENCES
1. Gove PB. Websters Third New International Dictionary, Unabridged. New York, NY:
Merriam-Webster; 2002.
2. Case records of the Massachusetts General Hospital.Weekly clinicopathological exercises.
Case 39-1995. A 72-year-old man with exertional dyspnea, fatigue, and extensive
ecchymoses and purpuric lesions. N Engl J Med 1995;333:1695-1702.
3. Lee RV. Scurvy: A contemporary historical perspective (in three parts). Conn Med
1983;47:629-632,703-704; Conn Med 1984;48:33-35.
-
7/27/2019 A Case of Scurvy in an Elderly Patient
6/8
4. Smith MS. The diagnosis and treatment of scurvy: An historical perspective. J R Nav Med
Serv 1986;72(2):104-106.
5. Porter R, ed. Cambridge Illustrated History of Medicine. Cambridge, England: University
Press; 1996:17, 46-7, 53, 192, 255-256, 268, 379.
6. Hurlimann R, Salomon F. Scurvy-A mistakenly forgotten disease. Schweiz Med
Wochenschr 1994;124(31-32):1373-1380.
7. Hampl JS, Johnston CS, Mills RA. Scourge of black-leg (scurvy) on the Mormon trail.
Nutrition 2001;17(5):416-418.
8. Stewart CP, Guthrie D, eds. Linds Treatise on Scurvy: A Bicentenary Volume Containinga Reprint of the First Edition of A Treatise of the Scurvy by James Lind. Edinburgh,
Scotland: University Press; 1953.
9. Levine M. New concepts in the biology and biochemistry of ascorbic acid. N Engl J Med
1986;314:892-902.
10. Clemetson CA. Barlows disease. Med Hypotheses 2002;59(1):52-56.
11. Hodges RE, Hood J, Canham JE, et al. Clinical manifestations of ascorbic acid deficiencyin man. Am J Clin Nutr 1971;24:432-443.
12. Kinsman RA, Hood J. Some behavioral effects of ascorbic acid deficiency. Am J Clin
Nutr 1971;24:455-464.
13. DeSantis J. Scurvy and psychiatric symptoms. Perspect Psychiatr Care 1993;29(1):18-22.
14. Reuler JB, Broudy VC, Cooney TG. Adult scurvy. JAMA 1985;253:805-807.
15. Hood J, Hodges RE. Ocular lesions in scurvy. Am J Clin Nutr 1969;22:559-567.
16. Hood J, Burns CA, Hodges RE. Sjgrens syndrome in scurvy. N Engl J Med
1970;282:1120-1124.
17. Hood J. Femoral neuropathy in scurvy. N Engl J Med 1969;281: 1292-1293.
18. Abboud FM, Hood J, Hodges RE, Mayer HE. Autonomic reflexes and vascular reactivity
in experimental scurvy in man. J Clin Invest 1970;49:298-307.
-
7/27/2019 A Case of Scurvy in an Elderly Patient
7/8
19. Shafar J. Rapid reversion of electrocardiographic abnormalities after treatment in two
cases of scurvy. Lancet 1967;2:176-178.
20. Sament S. Cardiac disorders in scurvy. N Engl J Med 1970;282:282-283.
21. Levine M, Conry-Cantilena C, Wang Y, et al. Vitamin C pharmacokinetics in healthy
volunteers: Evidence for a recommended dietary allowance. Proc Natl Acad Sci USA
1996;93:3704-3709.
22. Hodges RE, Baker EM, Hood J, et al. Experimental scurvy in man. Am J Clin Nutr
1969;22:535-548.
23. Levine M, Rumsey SC, Daruwala R, et al. Criteria and recommendations for vitamin Cintake. JAMA 1999;281(15):1415-1423.
24. Padayatty S, Levine M. New insights into the physiology and pharmacology of Vitamin
C. CMAJ 2001;164(3):353-355.
25. Johnston CS, Thompson LL. Vitamin C status of an outpatient population. J Am Coll
Nutr 1998;17:366-370.
26. Johnson CS, Solomon RE, Corte C. Vitamin C status of a campus population: College
students get a C minus. J Am Coll Nutr 1998;46(5):209-213.
27. Ellis CN, Vanderveen EE, Rasmussen JE. Scurvy. A case caused by peculiar dietary
habits. Arch Dermatol 1984;120:1212-1214.
28. Sherlock P, Rothschild EO. Scurvy produced by a Zen macrobiotic diet. JAMA
1967;199:794-798.
29. Schorah CJ, Morgan DB, Hullin RP. Plasma vitamin C concentrations in patients in a
psychiatric hospital. Hum Nutr Clin Nutr 1983;37:447-452.
30. Baumbach J. Scurvy by any other name: A case report. R I Med 1994;77(1): 24-25.
31. Ahmad K. Scurvy outbreak in Afghanistan prompts food aid concern. Lancet
2002;359(9311):1044.
-
7/27/2019 A Case of Scurvy in an Elderly Patient
8/8
32. Fauci AS, Braunwald E, Isselbacher KJ, et al, eds. Vitamin deficiency and excess.
Harrisons Principles of Internal Medicine. 14th ed. New York, NY: McGraw-Hill;
1998:484-485.