These symptoms may be described in infantile beriberi:

Hoarseness, where the child makes moves to moan, but emits no sound or just faint moans caused by nerve paralysis
Weight loss, becoming thinner and then marasmic as the disease progresses
Vomiting
Diarrhea
Pale skin
Edema
Ill temper
Alterations of the cardiovascular system, especially tachycardia (rapid heart rate)
Convulsions occasionally observed in the terminal stages

Cause
Beriberi is often caused by eating a diet with a very high proportion of calorie rich polished rice (common in Asia) or cassava root (common in sub-Saharan Africa), without much if any thiamine containing animals or vegetables.It may also be caused by shortcomings other than inadequate intake - diseases or operations on the digestive tract, alcoholism, dialysis or genetic deficiencies. All those causes mainly affect the central nervous system, and provoke the development of  Wernickes encephalopathy. Wernickes disease is one of the most prevalent neurological or neuropsychiatric diseases. In autopsy series, features of Wernicke lesions are observed in approximately 2% of general cases. Medical record research shows that about 85% had not been diagnosed, although only 19% would be asymptomatic. In children, only 58% were diagnosed. In alcohol abusers, autopsy series showed neurological damages at rates of 12.5% or more. Mortality caused by Wernickes disease reaches 17% of diseases, which means 3.4/1000 or about 25 million contemporaries. The number of people with Wernickes disease may be even higher, considering that early stages may have dysfunctions prior to the production of observable lesions at necropsy. In addition, uncounted numbers of people can experience fetal damage and subsequent diseases.
Volatile anesthetic agents have been shown to increase renal sympathetic nerve activity (RSNA), which causes retention of salts and water, diminished renal blood flow (RBF) and an increase in serum renin levels, but not in antidiuretic hormone (ADH). Treatment
The management of AKI hinges on identification and treatment of the underlying cause. The main objectives of initial management are to prevent cardiovascular collapse and death and to call for specialist advice from a nephrologist. In addition to treatment of the underlying disorder, management of AKI routinely includes the avoidance of substances that are toxic to the kidneys, called nephrotoxins. These include NSAIDs such as ibuprofen or naproxen, iodinated contrasts such as those used for CT scans, many antibiotics such as gentamicin, and a range of other substances.Monitoring of kidney function, by serial serum creatinine measurements and monitoring of urine output, is routinely performed. In the hospital, insertion of a urinary catheter helps monitor urine output and relieves possible bladder outlet obstruction, such as with an enlarged prostate. Prerenal
In prerenal AKI without fluid overload, administration of intravenous fluids is typically the first step to improving kidney function. Volume status may be monitored with the use of a central venous catheter to avoid over- or under-replacement of fluid.