Beriberi classification
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:
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Overview
Classification
Beriberi is usually classified into two types based on the main system affected. The two forms may appear in the same patient, but one form dominates the disease phenotype.
| Affected Site | Course | Population | Presentation | |
|---|---|---|---|---|
| Wet beriberi | Cardiovascular System |
|
Individuals with chronic thiamine deficiency | - Heart failure (acute or chronic).
- Peripheral edema: due to weakened capillary beds in peripheral tissues leading to fluid leakage. |
| Dry beriberi | Peripheral nervous system | Usually follows a chronic disease course | Individuals with chronic thiamine deficiency | Polyneuritis and symmetric, ascending paralysis of the peripheral nerve systems. It first affects the sensory system (parasthesia), then the motor system (loss of tendon reflexes, followed by foot and wrist drop) |
| Infantile beriberi | Cardiovascular or nervous system | Infants between one and four months of age, nursed by thiamine-deficient mothers. | ||
| Wenicke-Korsakoff Syndrome | Brain | Two separate conditions: Acute (Wernicke's encephalopathy) or chronic presentations (Korsakoff psychosis) | Chronic alcoholics |
- Wet beriberi usually affects the cardiovascular system, which may cause heart failure. Moreover, it weakens the capillary walls in peripheral tissues, causing tissue water leakage and edema; hence the nomenclature "Wet".
- Dry beriberi (or endemic neuritis) usually affects the nervous system, particularly the peripheral nerves, causing partial paralysis.[1]
Based on the disease course, wet beriberi can be further classified into two forms:
- Acute fulminant/pernicious form (Shoshin beriberi): This form is characterized by rapid onset, progressive disease course, and poor prognosis (often fatal). The heart is the main site affected and it usually leads to cardiovascular collapse.[2]
- Chronic wet beriberi: This form has a subtle onset and a gradual course and usually ends in high-output heart failure in three stages: Initial peripheral vasodilatation, followed by activation of the kidney renin-angiotensin system, leading to fluid overload, peripheral edema, and pulmonary effusion.
There are two forms of beriberi that occur in special populations due to their nature of risk factor exposure. "Infantile beriberi" occurs in children nursed by women deficient in thiamine and usually occurs between one and four months of age. Another form of the disease occurs mainly in chronic alcoholics "Wernicke-Korsakoff syndrome" in which the brain is the main target (cerebral beriberi). This form may have either acute (Wernicke's encephalopathy) or chronic presentations (Korsakoff psychosis).[3]
References
- ↑ "StatPearls". 2019. PMID 30725889.
- ↑ Meurin P (1996). "[Shoshin beriberi. A rapidly curable hemodynamic disaster]". Presse Med. 25 (24): 1115–8. PMID 8868953.
- ↑ Donnelly A (2017). "Wernicke-Korsakoff syndrome: recognition and treatment". Nurs Stand. 31 (31): 46–53. doi:10.7748/ns.2017.e10440. PMID 28351256.