Beri-beri - clinical diagnosis
Assessment of scurvy in emergency settings Zita 02.05.97
Beri-beri - clinical diagnosis Michael H.N. Golden 02.05.97
Beri Beri and rice André Briend 05.05.97
Re: Beri-beri - clinical diagnosis Michael H.N. Golden 03.06.97
Beri Beri in infants André Briend 04.06.97
Re: Beri Beri in infants Zita 04.06.97

Fri, 2 May 1997 10:48:30

from ( [])

Subject: Assessment of scurvy in emergency settings


I would be interested to know if anyone has more information on the following simpliflied 'field-friendly' (bedside) testing methods for vitamin C deficiency (or any other methods): (main source: Marks, J. A guide to the vitamins. Their role in health and disease. MTP. 1975)

- A dipstick test for estimation of vitamin C levels in the urine. Urine passed 4-6 hours after a 300 mg dose of ascorbic acid is collected and vitamin C levels are indicated by a characteristic colour change with 2,4-dinitrophenyl hydrazine.

- An intradermal dye test which depends on the power of the vitamin C of the skin to decolourize the blue, 2,6-dichlorophenolindophenol. A modification of this test involves the estimation of the rate of loss of colour when a drop of reagent is placed on the tongue. However, this test on its own is not considered specific enough.

I would also like to know about any 'field-friendly' methods (besides clinical methods) to detect/verify pellagra and beriberi in emergency settings.



Fri, 2 May 1997 13:23:29 +0100 (BST)

Subject: Beri-beri - clinical diagnosis

From: "Michael H.N. Golden" <>


The problem raised by Zita - confirmation of vitamin deficiency in the field, is incredibly important. Usually, there is no way of easily making the diagnosis. Cheap bedside/field methods that work would be invaluable. Work has not even been done on "specimenology" - how to preserve samples where there is no refrigeration for future analysis - surely we could develop the methods used in forensic medicine and neonatal screening to deal with dried blood spots sent by post from one country to another. I would urge us to put this at the top of our research agenda.


On the other hand the clinical skills that many have in making the diagnoses are woefully inadequate. After investigating a "reported" outbreak of beri-beri in West Africa in October, I wrote the following paper which is going to be published in Fiona O'Reilly's/ Jeremy Shoham's newsletter. Not only do I believe that beri-beri is often wrongly diagnosed, I also think that we are missing many cases - particularly of infantile beri-beri. I copy it here and would be very grateful for comments - particularly from those with personal experience of dealing with patients with beri-beri.


Recently the NGO community in West Africa learnt of an outbreak of Beri-Beri in an area with severe nutritional deprivation. The diagnosis had been based upon the presence of epidemic oedema found during a nutritional survey: the survey team included experienced doctors. I accompanied an ACF team, working in the area, to examine these patients. The only clinical feature that these patients had that resembled beri-beri was the oedema. The patients had "famine oedema" which is the same as adult kwashiorkor; exactly as described during the second world war and in the "Minnesota experiments" with volunteers. In the absence of diagnostic laboratories, the diagnosis of nutritional deficiency diseases depends upon 1) a high index of suspicion, 2) knowledge of the likely deficiencies in different circumstances and 3) the clinical skills, knowledge and experience to elucidate the characteristic clinical features of a deficiency. Clinical acumen is the most important. This paper addresses beri-beri which is primarily due to thiamine (vitamin B1) deficiency. Most forms of beri-beri are easily confused with other illnesses and are frequently missed in clinical practice unless classical wet, dry or aphonic beriberi is recognised,

When to suspect beri-beri.

Beri-beri occurs where there is a high carbohydrate or alcohol intake and a low thiamine intake. This classically occurs with polished rice, particularly where the rice is contaminated with moulds, and in alcoholism. However, raw fish and some "bush" teas or vegetables contain anti-thiamine enzymes that can precipitate beri-beri. The energy intake is usually good and energy expenditure high - beri-beri is not a typical feature of starvation.

Types of beri-beri.

Beri-beri causes cardiovascular and neurological signs and symptoms. There are eight clinically recognisable syndromes - five in adults and three in children. Often a patient has features of more than one of the syndromes. Beri-beri beard no relationship to anthropometric status - fat people get beri-beri; it also occurs in the fully-breastfed infant.

The resistance between the arteries and the veins drops to such an extent that the blood flows round the body much more rapidly than normal, the heart is unable to maintain this high output and fails.

These patients have oedema, a hyperdynamic circulation and a large heart. The patients are restless and their arms and legs feel warm to touch. The pulse pressure is high with an increase in the systolic pressure and a decreased diastolic pressure (eg 140/40); when the wrist encircled lightly the pulse is easily felt (water hammer pulse), slight pressure on the nails so that they go white shows pulsation in the nail bed.; the jugular venous pulse (in the neck) is raised with pronounced pulse waves; the apex of the heart is displaced to the left so that it may reach the axilla and it is easily felt; there are usually systolic "flow" murmurs and a third heart sound giving a "galloping" rhythm that is accentuated when the patient lies on the left side and breaths in. Unlike other forms of heart failure the patient's lungs are usually clear, they can lie flat on their backs without getting breathless and they are not cyanosed. The oedema needs to be differentiated from 1. Famine oedema (adult kwashiorkor), 2. nephritis, 3 nephrotic syndrome, 4 intoxication (heavy metals, ethylene glycol, etc). The hyperdynamic circulation can also be caused by 1 severe anaemia, 2 thyrotoxicosis, 3 pregnancy, 4 chronic liver disease, 5 strongyloidiasis, and 6 arteriovenous fistulae.

The heart is primarily affected and these patients have classical heart failure and sudden death. These patients are more breathless when the lie down and have crepitations in their lower lung fields. The incidence of Shoshin beri-beri in areas with an outbreak of wet beri-beri is unknown because it is not recognised and the death ascribed to some other cause of heart failure.

In dry beri-beri there is a peripheral neuritis. It starts with parathesia of the feet, diminished touch sensation, and a feeling of "heat" in the feet. Joint position, vibration and pain sensation are usually normal. The ankle and then the knee reflexes are lost and the patients have muscle weakness starting with the foot.

This is characterised by profound loss of recent memory, with preservation of past memory and an active imagination. These patients concoct very plausible stories about what they themselves (not other people) have been doing, to cover their memory defect and do not admit to any loss of memory (called "confabulation"). It is necessary to know what the patient has actually been doing before the history is taken. The defect is irreversible with thiamine treatment, but its progression is stopped.

These patients start with irritability and forgetfulness, progress to having, drooping of their eye lips (ptosis), squints where the eye does not move outwards (opthalmoplegia), horizontal flickering of the eyes (nystagmus), and other cranial nerve lesions, the patients may have an unsteadiness of their hand and food moments (cerebellar ataxia); they then progress to confusion and delirium before death. It is characterised by damage or destruction of small organs on the base of the brain (mamillary bodies) that control eye movements. Minor forms are quite common - up to 10% of post-mortem examinations in Australia show damage to the mamillary bodies. These patients are often misdiagnosed as other forms of encephalopathy such as viral illness, cerebral malaria, sleeping sickness, etc.

The peak prevalence of this form occurs in fat breast fed babies of 1-3 month of age. The first signs appear like colic with screaming bouts, restlessness, anorexia and vomiting. This progress to oedema, cyanosis and breathlessness with signs of heart failure. Increased pulse rate, enlargement of the heart, additional heart sounds, a systolic murmur, pulmonary oedema, liver enlargement and low urine volume. The children die from heart failure: the correct diagnosis is rarely made. Typhoid, malaria, pneumonia and septicaemia are commonly confused with this form of beri-beri.

The peak prevalence is in 4-6 month old children. The child's voice changes so that the cry gets more and more hoarse until no sound at all is produced. Strikingly, these children do appear to be crying without any noise. Without treatment they progress over a few days to restlessness, oedema, breathlessness and then death.

This usually occurs in 6-12 month old and is the equivalent of Wernickie's encephalopathy in the infant. The patient appears to have encephalitis/meningitis. There is nystagmus, muscle twitching, a bulging fontanelle, convulsions and unconsciousness. When a lumbar-puncture is done the cerebro-spinal fluid appears to be "gin" clear and does not froth easily when it is shaken. This can be confused with all forms of encephalitis and meningitis, malaria and even acute vitamin A intoxication.

Older children get the same features as adults.


What to do when beri-beri is suspected.

After you have carefully examined the patient and described the findings in all the systems, then you should give "flooding doses" of thiamine (normal adult requirement is 0.4mg per 1000 kcal). Give 50 or 100 mg thiamine hydrochloride intravenously and then give 10 mg per day orally. Infants may be treated with adult doses (it is not toxic in very large quantities), or lesser doses if this is more convenient. Mothers of patients should always be given 10mg per day orally.

The response is rapid in wet and infantile beri-beri. A diuresis quite suddenly starts between 4 and 48 hours after the thiamine (it is unclear why the delay occurs). It is dramatic with visible resolution of much of the oedema over 4 to 8 hours followed by complete loss over the next 48 hours. Shoshin and infantile cardiac beri-beri also respond dramatically with resolution of the heart failure. The convulsions and delirium in encephalitic responds rapidly and the patient's life is saved. However, the cranial nerve lesions can take months to recover and may be permanent. Aphonia gradually resolves over 2 to3 weeks. The mental changes is Korsakoff's psychosis are permanent and do not respond to treatment.

In population surveys urinary thiamine of less than 65 ug/g creatine indicates thiamine deficiency. This is not useful for individuals, where a red-cell transketolase or a lactate tolerance test is done - it may be suspected from a high anion-gap in the blood electrolyte profile.

Thank you!

Best wishes,


Prof. Michael H.N.Golden

Date: Mon, 5 May 1997 12:15:37 +0200 (METDST)

From: (Andre' BRIEND)

Subject: Beri Beri and rice


A short comment to Mike's note regarding Beri-beri

Beri beri is usually associated with a diet based on polished rice. To be more precise, there is a risk with the use of polished NON PARBOILED rice.

Beri beri is unknown in large parts of Asia with polished rice as staple food but where parboiling rice is part of the tradition.


Dr. André Briend

INSERM U 290, Hopital Saint Lazare, 107 rue du Faubourg Saint Denis, 75 475 Paris Cedex 10, France

tel 33-1-45 23 24 07; tel (direct) 33-1-48 00 56 04 fax 33-1-47 70 28 35

Tue, 3 Jun 1997 18:03:57 +0100 (BST)

Subject: Re: Beri-beri - clinical diagnosis

From: "Michael H.N. Golden" <>


>CallananatWFP.ORG says

>Thank you for the very interesting paper on beri beri. I wish to know

>how an entirely breast fed fat child could get beri beri? Low maternal



You might have seen the publications on the concept of type I and type II nutrients published in ACCSCN last year. It seems that this dichotomy of response also applies to breast milk. The concentration of type II nutrients (protein, potassium, sodium, chloride, phosphorus, zinc, magnesium) are regulated within a fairly narrow band in breast milk. The type I nutrients vary over a much wider range and will reflect the maternal intake much more closely. YES the answer to infantile beri-beri is that the breast milk thiamine content can drop to very low levels when mothers are on a deficient diet. It is uncommonly recognised.


Best wishes,

Prof. Michael H.N.Golden

Wed, 4 Jun 1997 15:56:23 +0200 (METDST)

From: (Andre' BRIEND)

Subject: Beri Beri in infants


A few years ago, a MSF group working in Thailand was intrigued by an epidemic of "sudden deaths" among breast fed infants in a rice eating population of Burmese refugee (rice was polished and not parboiled). This epidemic was important enough to give an unusual peak of deaths around 3 months of age (usually, mortality declines from the first day of life, provided you have no neo natal tetanus which occurs below 1 month anayway). This was investigated in some details and low vitamine B1 levels were found in breast milk samples. The most likely explanation was that it was infatile beri beri.

I don't know whether this was ever published but I am sure the report must be in MSF /Epicentre. The lesson was that apparently you may have an increased mortality at the population level from infant beri beri before a proper diagnosis is made. Clinical diagnosis is not so obvious in young infants (easier though with the last issue of ENN field exchange).

Sorry for badly quoting from memory. Does anybody have the report ?


Dr. André Briend

From: Zita,

Date: Wed, 04 Jun 97 16:33:17 +0100

Subject: Re: Beri Beri in infants


There is a short article re: beriberi in infants in Thailand in the MSF Medical News, Vol 1, #4, August 1992 with the following title:

'Study of the food habits of breast-feeding women among the Karen refugee population in the Mae Sod region, Thailand, 1992.'

A very interesting report. The thiamin levels of breast milk were measured, however, when the report was written, the lab results were not out yet. I would be very interested in having the lab results if they are available.

Regards, Zita