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Beriberi differential diagnosis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Abdelrahman Ibrahim Abushouk, MD[2]

Overview

Beriberi should be differentiated from other causes of cardiac dysfunction (wet beriberi), peripheral neuropathy (dry beriberi), delirium (Wernicke-Korsakoff syndrome) andexcessive alcohol drinking. However, the differential diagnosis is broad due to the non-specific symptoms of cardiac and neural involvement associated with the condition.

Differentiating Beriberi from other Diseases

Beriberi should be differentiated from other causes of cardiac dysfunction (wet beriberi), peripheral neuropathy (dry beriberi), delirium (WKS), and other disorders caused by excessive alcohol drinking. However, the differential diagnosis is broad due to the non-specific symptoms of cardiac and neural involvement associated with beriberi.[1][2][3]

Disorders Etiology Clinical Presentation Laboratory findings
Cardiomyopathy due to other causes as alcohol or DM
  • Dyspnea/Orthopnea
  • Edema
  • Syncope
  • Palpitations
Delirium and delusional disorders
  • Acute liver failure
  • Acute metabolic and electrolyte disturbances
  • Infections/sepsis
  • Toxins/drug overdose
  • Disturbed attention
  • Poor cognition
  • Impaired psychomotor activity
  • Emotional instability
Nerve entrapment disorders Chronic injuries to nerves as they pass between bones and ligaments:
  • Carpal tunnel syndrome
  • Cubital tunnel syndrome
  • Suprascapular nerve compression
  • Meralgia Paresthetica (lateral femoral cutaneous nerve)
Within the distribution of the affected nerve, the patient may complain of:
    • MRI short inversion imaging recovery (STIR) technique
    Alcoholic hepatitis
    • Chronic and excessive alcohol consumption
    • Increased serum levels of ALT and AST
    • Blood picture: Leukemoid reactions (high WBCs count) may be present.
    • Liver US: Changes in liver size and dilatation of hepatic veins.
    Diabetic ketoacidosis In patients with type 1 DM, exposed to:
    • Poor insulin compliance
    • Infections/sepsis
    • Stress
    • Idiopathic
    • Hyperglycemia
    • Lower PH and bicarbonate levels
    • Ketonemia and ketonuria
    • Electrolyte disturbances
    • Impaired renal function
    Hyperthyroidism
    • Elevated T3 and T4 hormones
    • TSH: Reduced in 1ry and Elevated in 2ry hyperthyroidism.
    • Thyroid stimulating antibodies: Elevated only in Grave’s disease
    Folic acid deficiency
    • Palpitations
    • Headache
    • Fatigue
    • Poor appetite
    • Sore tongue
    • Low serum folate <2.5ng/ml
    • CBC: Macrocytic anemia and low correlated reticulocyte count
    • Peripheral blood smear: Neutrophil granulocytes and anisocytosis

    References

    1. Whitfield KC, Bourassa MW, Adamolekun B, Bergeron G, Bettendorff L, Brown KH; et al. (2018). “Thiamine deficiency disorders: diagnosis, prevalence, and a roadmap for global control programs”. Ann N Y Acad Sci. 1430 (1): 3–43. doi:10.1111/nyas.13919. PMC 6392124. PMID 30151974.
    2. DiNicolantonio JJ, Liu J, O’Keefe JH (2018). “Thiamine and Cardiovascular Disease: A Literature Review”. Prog Cardiovasc Dis. 61 (1): 27–32. doi:10.1016/j.pcad.2018.01.009. PMID 29360523.
    3. Chandrakumar A, Bhardwaj A, ‘t Jong GW (2018). “Review of thiamine deficiency disorders: Wernicke encephalopathy and Korsakoff psychosis”. J Basic Clin Physiol Pharmacol. 30 (2): 153–162. doi:10.1515/jbcpp-2018-0075. PMID 30281514.


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