![]() |
|||
|
|||
Persistent anaemia due to scurvy
Vincent Ho, Pieter Prinsloo, John Ombiga
We present a case of a 45-year-old man from Papua New Guinea
who presented with anaemia. A bleeding duodenal ulcer was thought initially to
be the sole cause of his anaemia but when his anaemia did not resolve despite
haemostasis and blood transfusion another explanation had to be entertained.
Physical examination noted florid features of scurvy and a
poor dietary history was elicited. Scurvy is a rare clinical condition in modern
times and a high index of suspicion together with a good history and physical
examination is required to make a prompt diagnosis.
Case reportA 45-year-old man from Papua New Guinea presented to the
Cairns Base Hospital’s Emergency Department after being referred for
investigation and management of anaemia. He had complained of a painful swollen
right knee with limp and lethargy for the past 6 months. His local medical
officer had prescribed him diclofenac 50 mg three times daily for the past 2
weeks for analgesia. In the last few days prior to admission to hospital he
described epigastric pain and melaena. His past medical history was significant
only for depression. He denied frequent alcohol consumption.
Laboratory investigations noted normochromic normocytic
anaemia with a haemoglobin of 59 g/L. His white cell count, platelet count, and
coagulation profile were all normal. Iron studies revealed low serum iron levels
with high ferritin levels. Vitamin B-12 and folate levels were in the normal
range.
His anaemia was attributed to an upper gastrointestinal
bleed on the background of non-steroidal anti-inflammatory use. He was
transfused 4 units of packed cells, commenced on intravenous proton-pump
inhibitor therapy, and admitted for urgent endoscopy.
At endoscopy, a large duodenal ulcer was visualised and the
bleeding vessels at the base were clipped, providing haemostasis. His epigastric
pain and melaena resolved. In spite of this, over the next 3 days his
haemoglobin progressively dropped to 63 g/L. A repeat endoscopy did not show any
signs of repeat bleeding from the ulcer. Another cause for his anaemia was
sought.
Physical examination revealed that he had marked gingival
swelling and bleeding (Figure 1). His skin follicles were noted to have
increased pigmentation and this was later confirmed to be perifollicular
hyperkeratosis (Figure 2). His right leg was as hard as wood and he had
prominent ecchymosis of his thigh with a large right haemarthrosis.
Further enquiry regarding his diet revealed that he had a
very poor oral intake for many months and virtually took no vegetables or fruit.
Scurvy was suspected as the clinical diagnosis.
His plasma ascorbic acid level recorded as 5 micromol/L
(normal range 20–120 micromol/L) thus confirming vitamin C deficiency.
Figure 1. Gingival swelling and bleeding in our
patient with scurvy
![]() Figure 2. Prominent classical perifollicular
hyperkeratosis seen in scurvy
![]() He was commenced on vitamin C 250 mg three times daily and
his dentition, ecchymosis, and haemarthrosis improved rapidly. His full blood
count quickly normalised. He was discharged on an oral proton-pump inhibitor,
given advice regarding a healthy diet, and follow-up with a dietician was
arranged.
DiscussionScurvy is traditionally found in impoverished populations,
people on ‘fad’ diets, alcoholics, and those with psychiatric
disturbances.1 Centuries ago it was common in
sailors on extended voyages due to the lack of fresh fruit and vegetables on
board. Initial presenting symptoms are generally non-specific and include
weakness, anorexia, depression, and
lassitude.2
The diagnosis of scurvy is based on the finding of specific
clinical features supported by a consistent dietary history. A plasma vitamin C
level of below 11 micromol/L supports the diagnosis of scurvy, as it corresponds
to a total body store of less than 300 mg.2,3
As a result of defective collagen biosynthesis due to
ascorbic acid deficiency, blood vessel fragility manifests as petechiae,
purpura, and large ecchymoses.4 Haemarthroses
of the knee have been described.5,6
Bleeding gums and gingivitis are prominent in individuals
with pre-existing periodontal disease. Dermatological features include broken
and coiled hairs (due to abnormal collagen formation), and perifollicular
haemorrhages and hyperkeratosis.7 Anaemia is
seen in 75% of cases of scurvy, with iron and folate deficiencies as
contributing factors.8
The institution of treatment for scurvy is simple. Oral
vitamin C supplementation leads to dramatic and rapid improvement in symptoms,
with clinical manifestations disappearing within weeks.
Our case illustrates that even if a case of anaemia appears
obvious, for example a classic picture of a gastrointestinal bleed, it is
imperative to search for other causes if the anaemia still persists despite
correction.
Scurvy is a rare clinical condition which can account for
persistent anaemia if untreated, and a high index of suspicion with a good
history and examination is required to make a prompt diagnosis in order to not
delay treatment.
Author information: Vincent Ho, Clinical
Lecturer in Medicine, James Cook University, Cairns Base Hospital, Cairns,
Queensland, Australia; Pieter Prinsloo, General Surgeon, Cairns Base Hospital,
Cairns, Queensland, Australia; John Ombiga, Gastroenterologist, Cairns Base
Hospital, Cairns, Queensland, Australia
Correspondence: Dr Vincent Ho, Department
of Medicine, Cairns Base Hospital, Cairns, Queensland, Australia 4870. Email: Vincent_Ho@health.qld.gov.au
References:
|
|||
| Current
issue | Search journal |
Archived issues | Classifieds
| Hotline (free ads) Subscribe | Contribute | Advertise | Contact Us | Copyright | Other Journals |