The development of beriberi, its symptoms and its
pathology are extremely variable, making it diffi cult
to describe a clinical picture or sequence of development.
Many of the early writers described three forms
of beriberi in adult humans: dry (wasting) and wet
(oedematous) beriberi, which are chronic forms, and
acute, fulminating (cardiac) beriberi. Which of these
forms predominates depends on the circumstances.
Vitamin B1 deprivation accompanied by malnutrition
and low physical activity tends to favour beriberi presenting
in the dry form, whereas high carbohydrate
intake and high physical activity during vitamin B1
deprivation predispose to wet beriberi. It should be
emphasized that any one of these forms may merge
Dry beriberi is a disease of the peripheral nervous
system involving bilateral impairment of sensory,
motor and refl ex functions. The pathological fi ndings
are segmental thinning of myelin in peripheral
nerves, progressing to degeneration of fi bre tracts.
The neuropathy begins in the feet and legs and then
extends up the body. Early signs of dry beriberi often
include sensations of pins and needles and numbness
in the feet. The legs, especially the calves, feel heavy
and weak so that walking becomes uncomfortable.
As the disease progresses, there is a marked wasting
of the leg muscles and even slight pressure applied to
the calves elicits severe pain. The characteristic foot
and wrist drop develop and there may be complete
fl accid paralysis of the lower, and occasionally upper,
In wet beriberi, vitamin B1 defi ciency affects the
cardiovascular system by causing arteriolar dilation
throughout the circulatory system and by weakening
the heart muscle. The vasodilation causes a two-fold
increase in the venous return of blood to the heart.
Physical signs of wet beriberi are indicative of highoutput
cardiac failure; they include tachycardia, rapid
circulation time, elevated peripheral venous pressure
and widespread oedema. Pathological changes are
an enlarged heart, swollen liver, and the presence of
fl uid in the pericardial, pleural and abdominal cavities.
Microscopically, the cardiac muscle fi bres show
fragmentation and hydropic degeneration with interstitial
The acute form of beriberi, known in Japan as
‘shoshin’, usually results in sudden death from heart
failure. The sufferer experiences severe dyspnoea,
violent palpitation of the heart and intense precordial
pain. The heart and liver become enlarged and there is
neck vein distension, cyanosis and extreme tachycardia.
Oedema is variable in this form of beriberi.
Infantile beriberi occurs in breast-fed babies between
the second and fi fth month of life. The mother
may display no signs of beriberi although obviously
her milk must be of low vitamin B1 content through
poor diet. As in adults, several clinical syndromes may
occur and the condition may be chronic or acute.
Vomiting is one of the most important early signs of
infantile beriberi. In severe cases the child appears to
be crying but no sound is heard or only a thin whine.
This characteristic feature, aphonia, is due either to
paralysis of the laryngeal nerve or to oedema of the
vocal cords. A chronic, pseudomeningeal form of
beriberi which affects the central nervous system and
may cause convulsions occurs in older infants aged 7
to 9 months.